f)>^ 


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7  7/3 

CoUege  of  ^{jps^tciansf  anb  ^urgeonsi 
Eibrarp 


GIFT  OP 

Frederick  S.  Lee 


s^^^l^ 


THE    DIAGI^OSIS 

.       OF 

JSTERYOUS    DISEASES 


BY 

PURVES  STEWART,  M.A.,  M.D.  Edin.,  F.R.C.P. 

PHYSICIAN  TO   OUT-PATIENTS  AT   THE  WESTMINSTER  HOSPITAL  ;  JOINT-LECTUREK  ON 

MEDICINE    IN    THE    MEDICAL    SCHOOL  ;     PHYSICIAN    TO    THE  WEST    END 

HOSPITAL    FOR    NERVOUS   DISEASES,    AND    TO    THE    ROYAL 

NATIONAL  ORTHOPAEDIC  HOSPITAL  ;   CONSULTING 

PHYSICIAN   TO  THE   CENTRAL  LONDON 

THROAT   HOSPITAL 


THIRD  EDITION,   REVISED  AND  ENLARGED  i 
SECOND  IMPRESSION 


NEW   YORK 
E.    B.    TREAT    &    CO. 

LONDON:   EDWARD   ARNOLD 
1913 

[All  rights  reserved] 


K. 


(t5^'i 


\V2 


PREFACE   TO   THE    THIIID   EDITION 

It  is  seldom  in  practice  that  we  meet  with  diseases  in  their 
fully-developed,  so-called  "  typical"  forms  ;  more  often  we  have 
to  deal  with  patients  who  exhibit  signs  and  symptoms  common 
to  several  diseases.  This  volume  approaches  the  subject  of 
diagnosis  of  nervous  diseases  from  the  clinical  standpoint, 
avoiding  abstruse  details  of  purely  theoretical  interest. 

The  last  edition,  published  in  1908,  reappeared  in  1910  in 
French  and  German  translations,  the  work  of  the  late 
Professor  Gustave  Scherb  (Algiers)  and  of  Dr.  Karl  Hein 
(Bad  Schonfliess)  respectively.  These  foreign  editions  have 
had  the  advantage  of  introductory  prefaces  by  Dr.  F. 
Helme  of  Paris  and  Professor  Eduard  Mliller  of  Marburg. 
To  all  these  gentlemen  I  would  here  express  my  grateful 
appreciation. 

The  present  edition  has  been  revised  throughout  and 
a  number  of  new  figures  have  been  added,  together  with 
a  considerable  amount  of  fresh  material  in  the   text. 

The  subject  of  the  work  is  mainly  that  of  diagnosis ; 
treatment  is  not  discussed  save  incidentally  here  and  there. 
The  order  pursued  is  that  in  which  it  is  convenient  to  study 
phenomena  during  the  process  of  diagnosis.  All  the  clinical 
illustrations  are  from  cases  which  I  have  observed  personally 
in  hospital  or  private  practice, 

I  hope  that  the  book,  despite  imperfections  of  which  I  am 
conscious,  will  continue  to  be  useful  to  the  advanced  student 
and  to  the  practitioner,  not  to  replace  but  to  supplement  the 
text-books  already  in  use. 

Once  more  I  have  to  express  my  gratitude  to  my  col- 
leagues, both  at  Westminster  and  at  the  West  End  Hospital, 
for  their  kindness  in  permitting  me  to  study  various  cases 


iv  PREFACE 

under  their  charge.  In  particular  I  would  acknowledge  the 
kindness  of  my  colleague  Dr.  Harry  Campbell,  who  allowed 
me  to  photograph  the  brain  shown  in  Fig.  223.  I  am  also 
indebted  to  Dr.  James  Mackenzie  and  to  Dr.  Dundas  Grant  for 
many  useful  suggestions. 

Lastly,  my  warmest  thanks  are  again  due  to  Dr.  S.  A. 
Kinnier  Wilson  for  his  invaluable  criticism  and  help  in  the 
correction  of  the  proof-sheets. 

PURVES  STEWART. 


94  Haeley  Street,  London,  W. 
September  1911. 


CONTENTS 


I.  Anatomy  and  Physiology 
II.  Anatomy  and  Physiology  {continued)    . 

III.  Method  of  .Case-Taking 

IV.  Coma         

V.  Fits  and  other  Convulsive  Phenomena 

VI.  Involuntary  Movements 
VII.  Aphasia  .... 
VIII.  Disorders  oe  Articulation 
IX.  Cranial  Nerves 
X.  Cranial  Nerves  {continued) 
XI.  Pain  and  other  Abnormal  Subjective  Sensations 
XII.  Abnormalities     of     Sensation  :    Hyper.esthesia, 
^sthesia,  Anesthesia 

XIII.  Organic  Motor  Pahalysis  of  Upper  Neurone  Ty'pe 

XIV.  Organic  Motor  Paralysis  of  Lower  Neurone  Type 
XV.  Recurrent  and  Transient  Palsies     . 

XVI.  Inco-ordination 

XVII.  Postures  and  Gaits 

XVII [.  Tropho-Neuroses 

XIX.  Reflexes 

XX.    AlPFECTIONS   OP   THE    SYMPATHETIC.      AnGIO-NeUROSES 

XXI,  The  Neuroses 

XXII.  Electro-Diagnosis  and  Electro-Prognosis 

XXIIT.  The  Cerebro-Spinal  Fluid 

XXIV.  Disorders  of  Sleep 

XXV.  Intra-Cranial  Tumours 

INDEX , 


Par- 


page 
] 

27 

48 

55 

65 

79 

95 

109 

118 

148 

173 

190 
206 
222 
248 
257 
267 
290 
316 
334 
355 
389 
403 
423 
434 

455 


Digitized  by  the  Internet  Archive 

in  2010  with  funding  from 

Open  Knowledge  Commons 


http://www.archive.org/details/diagnosisofnervoOOpurv 


PLATES 

I.    Sub-ungual  hsemorrhages  of  the  hand   .         .         .To  face  page      304 
II.  Erythromelalgia >i         »  350 


THE    DIAGNOSIS    OF    NERVOUS 
DISEASES 

CHAPTER   I 

ANATOMY    AND    PHYSIOLOGY 

There  is  no  department  of  medicine  where  an  accurate  knowledge 
of  anatomy  is  of  greater  importance  than  in  the  diagnosis  of 
nervous  diseases.  Let  us  therefore,  at  the  outset,  recall  some  of 
the  main  points  in  the  anatomy  and  physiology  of  the  nervous 
system. 

The  nervous  system  consists  of  two  main  divisions  : — (1)  the 
cerebro-spinal,  comprising  the  brain  and  spinal  cord,  together 
with  the  cranial  and  spinal  nerves,  and  (2)  the  sympathetic, 
constituted  by  two  chains  of  pre-vertebral  ganglia,  one  on  each 
side  of  the  spine.  These  two,  the  cerebro-spinal  and  sympathetic, 
intercommunicate. 

For  teaching  purposes  it  is  convenient  to  regard  the  nervous 
system  as  built  up  of  nerve-cells,  and  their  processes  the  nerve- 
fibres.  Both  are  excitable.  But  whereas  the  nerve-cell  has 
been  commonly  assumed  to  originate  impulses  as  does  the 
cell  of  an  electric  battery,  the  nerve-fibres  serving  merely  as 
conductors,  it  is  unusual  for  an  impulse  to  arise  within  a 
nerve-cell,  except  as  the  result  of  a  transmitted  impulse.^  Each 
nerve-fibre  is  made  up  of  a  bundle  of  extremely  fine  neuro- 
fibrillse  which  traverse  the  nerve-cell,  entering  it  through  one  process 
and  leaving  it  through  another.  In  this  way  the  nerve-cell  acts 
as  a  convenient  shunt  for  impulses,  receiving  them  from  one 
quarter  and  transmitting  them  to  another.     The  nerve-cell  also 

1  The  cardiac  and  respiratory  nuclei  in  the  medulla  are  exceptions  to  tliis 
rule.  These  automatic  centres  can  be  stimulated,  not  only  by  transmitted 
nerve-impulses,  but  also  by  chemical  changes  in  the  blood,  e.g.  by  deficiency 
of  oxygen  and  excess  of  CO.,  or  of  lactic  acid. 

A 


2  NERVOUS   DISEASES 

exerts  a  trophic  influence  over  the  nerve-fibre  and  is  intimately 
concerned  with  its  nutrition,  so  that  the  nerve-fibre  degenerates 
if  separated  from  its  trophic  nerve-cell. 

In  a  reflex  motor  act,  which  is  the  simplest  manifestation  of 
nervous  energy,  as  for  example  in  the  plantar  reflex,  the  impulse 
or  stimulus  starts  from  a  sensory  end-organ,  in  this  instance  the 
skin  of  the  sole.  The  impulse  travels  up  a  sensory  nerve-fibre, 
through  the  corresponding  posterior  nerve-root  into  the  spinal 
cord,  and  there,  through  the  intermediation  of  another  inter-com- 
municating nerve -fibre  and  cell  in  the  grey  matter  of  the  cord. 


Post,  nerye  root 


Skzrv 


Muscle. 


Fig.  1. — Diagram  of  a  Simple  Spinal  Keflex. 


it  reaches  an  anterior  cornual  cell.  From  this  motor-cell  an 
efferent  impulse  starts,  travelling  outwards  along  an  anterior 
nerve-root  into  a  peripheral  nerve  and  thus  reaching  a  muscle-fibre 
in  the  flexor  muscle  of  the  toes.  The  muscle  contracts  and  with- 
draws the  sole  of  the  foot  from  the  original  irritant. 

The  accompanying  diagram  (Fig.  1)  will  serve  to  recall  the  chief 
components  of  a  simple  spinal  reflex,  such  as  we  have  just  described. 

Some  reflexes  occur  unconsciously,  as  for  example  the  reflex 
contraction  of  the  pupil  when  the  retina  is  stimulated  by  light, 
or  again,  the  normal  movements  of  the  stomach  and  intestines. 
But  in  other  cases  the  afferent  impulse,  besides  exciting  a  reflex 
motor  action,  sends  part  of  its  impulse  upwards  to  the  higher 
centres  of  the  opposite  cerebral  cortex,  where  it  produces  a  con- 
scious sensation.    This  is  accomplished  by  means  of  a  sensory  fibre 


ANATOMY    AND    PHYSIOLOGY 


passing  upwards  in  the  substance  of  the  spinal  cord,  as  indicated 
in  the  other  diagram  (Fig.  2),  through  relays  of  nerve-cells  and 
fibres  in  the  medulla,  pons,  and  so  on,  to  the  perceiving  centre  in 
the  cortex. 

Moreover,  a  discharge  of  motor  energy  from  the  motor  cell  in 


Ascending 

Se/isory  \ 

fibre       ' 


VoLurvbary 
Motor 
fd>re 


Skiw 


Muscle 

Fig.  2. — Diagram  of  a  Voluntary  Motor  Act. 

the  anterior  cornu  can  be  produced  not  only  reilexly,  from  below, 
but  also  voluntarily,  from  above.  This  is  achieved  by  an  impulse 
descending  from  the  cortical  motor  centre  of  the  opposite  side, 
through  the  crossed  pyramidal  tract  down  the  cord  to  the  anterior 
cornual  cell  (see  Fig.  2).  A  discharge  can  also  be  voluntarily 
inhibited  from  above. 

Confining  ourselves  now  to  the  consideration  of  a  cerebro-spinal 
reflex  motor  action,  we  must  bear  in  mind  that  afferent  impulses, 
on  reaching  the  cortical  sensory  centres,  do  not  necessarily  produce 
a  descending  impulse  along  the  pyramidal  tract.  If  they  do,  this 
is  simply  an  automatic  action,  or  a  longer  variety  of  reflex.    There 


4  NERVOUS    DISEASES 

exist  in  the  cortex  perceiving-centres  wMcli  take  cognisance  of  the 
source  and  nature  of  the  stimulus,  and  determine  whether  or  not  any 
active  notice  shall  be  taken  of  it,  that  is  to  say,  whether  a  voluntary 
(and  not  merely  an  automatic)  movement  shall  or  shall  not  take  place. 

Some  reflexes,  even  though  associated  with  conscious  sensory 
impressions  (for  example  the  vomiting  reflex,  or  the  sexual  reflex), 
cannot  be  inhibited.  This  is  possibly  owing  to  the  absence  of  anta- 
gonistic muscles  which  could  prevent  the  reflex.  Bat  other  reflexes 
can  be  inhibited  by  contracting  the  opposing  muscles  and  thereby 
fixing  the  part  which  would  otherwise  make  a  reflex  movement. 

Finally,  by  education,  a  motor  impulse  can  be  initiated  at  the 
cortical  motor  centre,  without  any  preceding  afferent  impulse 
from  the  part  to  be  moved.  All  movements  in  a  new-born 
infant  are  either  reflex  or  automatic,  and  only  gradually  does  the 
child  learn  to  call  in  antagonistic  muscles,  and,  by  an  effort  of 
the  will,  to  inhibit  reflex  acts  and  to  initiate  voluntary  ones. 

Certain  more  complicated  reflexes,  such  as  the  reflex  move- 
ments of  respiration,  have  their  centres  in  the  medulla  ;  others, 
such  as  the  reflex  movements  of  the  heart  and  blood-vessels,  have 
their  lower  reflex  centres  in  the  sympathetic  ganglia,  but  can 
also  be  influenced  by  the  cerebro-spinal  nervous  system.  Others 
again,  such  as  the  movements  of  the  heart,  stomach,  and  intestine, 
can  be  performed  independently  of  the  central  nervous  system. 

Figs.  3  and  4  are  diagrams  of  the  cerebral  cortex,  both  on  its 
convex  and  its  mesial  aspect.  It  is  unnecessary  here  to  enumerate 
in  detail  the  various  fissures  and  sulci,  or  the  different  lobes  and 
convolutions. 

When  we  look  at  a  brain,  the  first  landmarks  to  be  identified  are 
the  Sylvian  and  Rolandic  fissures.  The  central  or  Rolandic  fissure 
starts  at  the  middle  line  above,  from  a  point  half  an  inch  behind 
the  mid-point  between  the  nasion  and  the  external  occipital 
protuberance.  It  runs  downwards  and  forwards,  along  the  convex 
surface  of  the  brain,  in  the  direction  of  the  anterior  part  of  the 
horizontal  limb  of  the  Sylvian  fissure,  making  an  angle  of  about  67| 
degrees  i.e.  three-quarters  of  a  right  angle,  with  the  middle  line. 

These    two    figures   also   show    diagrammatically   our  present 


ANATOMY   AND    PHYSIOLOGY  5 

views  on  cerebral  localisation.  It  should  be  particularly  observed 
that  the  motor  areas  in  the  pre-central  convolution  extend  back 
as  far  as  the  Rolandic  fissure  but  not  behind  it,  as  was  formerly 
taught.  Not  only  by  experimental  stimulation  in  anthropoid  apes/ 
and  in  certain  cases  in  man,  but  also  by  histological  research,^  it 


Fig.  3. — Scheme  of  Cerebral  Localisation  (outer  surface). 


Fornix. 


Fig.  4. — Scheme  of  Cerebral  Localisation  (mesial  surface). 

has  been  shown  that  the  posterior  wall  of  the  Rolandic  fissure  differs 
in  function  and  structure  from  the  anterior  or  motor  wall.      The 

1  Sherrington  and  Griinbaum,  Trans.  Path.  Soc.  Lond.,  1902,  vol.  liii. 
p.  127. 

^  Campbell,  A.  W.,  Histological  Studies  on  the  Localisation  of  Cerebi-al 
Function,  1905. 

Brodmann,  K.,  Journ.  f.  Psychologic  und  Neurologic,  Bd.  ii.  p.  80. 


6  NERVOUS   DISEASES 

anterior  wall  possesses  giant  pyramidal  cells,  and  has  no  granular 
layer,  whilst  the  posterior  wall  has  a  distinct  granular  layer,  with 
no  giant  cells  (see  Fig.  5). 

Another  point  to  remember  is  that  the  different  so-called  motor 
areas  are  not  sharply  marked  off  from  one  another  like  a  mosaic, 
but  overlap,  each  area  in  Figs.  3  and  4  signifying  that  stimulation 
of  that  point  produces  the  maximum  movement  of  the  particular 


FwsTirej££oLando 


Fitr.  5. — Diagram  of  cellular  structure  of  pre-  and  post-central  convolutions 

( after' Vogt). 

part    mentioned.      Moreover,  there   are    minor  variations  in  the 
extent  of  the  various  centres  in  different  individuals. 

The  chief  path  by  which  motor  impulses  are  conducted  from  the 
cortical  motor  areas  to  the  muscles  is  the  pyramidal  tract,  whose 
course  is  diagrammatically  indicated  in  Fig.  6.  From  the  motor 
cells  in^^the  cortex  the  fibres  converge  through  the  corona  radiata 
into  the  great  strand  of  nerve-fibres  between  the  lenticular 
nucleus  externally  and  the  optic  thalamus  and  caudate  nucleus 
internally,  namely,  the  internal  capsule.  Fig.  7  shows  a  horizontal 
section  through  the  internal  capsule,  in  which  we  notice  that  it  has 
an  anterior  and  a  posterior  limb,  joining  each  other  at  an  obtuse 
angle,  the  genu  or  knee.      The  motor  fibres  for  the  leg  and  arm 


ANATOMY    AND    PHYSIOLOGY 

Leg 


Caudxxte  NibcLeus 
Optic  Th/xZcuTUhS' 

L  enticuLocrNiwle  us 


FULet- 
ReoLNacLeus -. 


6'^Nvu:leus 
FaciaLNvLcleiLS 
FUleb- 


CRUS  CEREBRI 
Level  of  ^""^Merve 


VONS 
Leveh  cfFobcial-Merye 

-Fojcialj  Nerve 


FiOet 
Fyramidi  — 


CrosseciPyranvidLaL  Tract 


Arm/  - 


FcLce. 


%     \>AEBUL,l.A 
Hypoalossoub  Nerve 

DirectFyrajnidjoL  Tract 
SPINAL  CORD 


Leg 


YiQ.  6.— Diagram  of  Pyramidal  Tract  and  its  course  through  the  brain 

and  cord. 


8  -  NERVOUS    DISEASES 

occupy  tlie  anterior  two-thirds  of  the  posterior  limb,  the  fibres  for 
the  tongue  and  mouth  are  at  the  genu,  those  for  the  face  just  in 
front.  But  the  order  in  which  these  different  strands  pass  through 
the  internal  capsule  is  not  quite  the  same  as  that  in  which  they 


CauoLaJb&IfttclevbS 


•JtenticularlliLcleiis 
Cloajustrunv 

Sensory  Fibres 
Sylvian/ Fijssiijre> 


VisuuxL  Fibres  oT 
Optic  S/udiaJULoTi,. 


Farleto-  Occipital  Fissure 


Fig.  7. — Horizontal  section  through  right  cerebral  hemisphere,  showing 
position  of  the  various  strands  in  the  internal  capsule.  (After  Beevor 
and  Horsier.) 


started  from  the  cortex.  Thus  we  notice  that  immediately  behind 
the  fibres  for  the  lips  we  have,  from  before  backwards,  those  for  the 
shoulder,  elbow,  and  fingers  (not  fingers,  elbow,  shoulder),  then  for 
the  trunk,  and  lastly  for  the  hip,  knee,  and  toes.  We  also  notice, 
in  passing,  that  the  pathway  (thalamo-cortical)  of  the  sensory  fibres 
traverses  the  posterior  part  of  the  capsule,  and  that  behind  them 


ANATOMY    AND    PHYSIOLOGY  9 

again  are  the  visual  fibres.  The  sensory  fibres  probably  do  not 
form  a  separate,  compact  bundle,  but  are  partially  mingled  with 
some  of  the  motor  fibres  for  the  leg. 

Before  leaving  Figs.  6  and  7,  it  is  of  interest  to  study  briefly, 
with  their  help,  the  difierent  effects  produced  by  lesions  of  the 
pyramidal  motor  tract  at  various  levels. 

A  lesion  in  or  near  the  motor  cortex,  if  moderate  in  size,  will 
produce,  according  to  its  situation,  a  monoplegia  of  the  face,  arm, 
or  leg,  on  the  opposite  side  of  the  body.  A  somewhat  larger  lesion 
will  produce  a  brachio-facial  or  a  brachio- crural  monoplegia.  From 
the  proximity  to  the  middle  fine  of  the  cortical  centres  for  the  leg, 
a  mesial,  or  bilaterally  symmetrical,  lesion  may  impHcate  the  leg 
centres  of  both  sides,  producing  a  diplegia,  mainly  affecting  the 
legs.  (We  observe  that  facio-crural  monoplegia  without  implication 
of  the  arm  is  impossible  from  a  single  lesion.)  For  the  production 
of  a  complete  hemiplegia  of  face,  arm,  and  leg  a  cortical  lesion  must 
be  very  extensive.  But  in  the  internal  ca-psule  all  these  strands 
are  closely  crowded  together,  so  that  a  moderate-sized  capsular 
lesion  can  produce  a  complete  hemiplegia,  whereas  a  capsular 
lesion  small  enough  to  cause  a  mere  monoplegia  is  well-nigh 
impossible. 

If  the  capsular  lesion  be  in  the  region  of  the  genu  we  have 
hemiplegia  of  face,  arm,  and  leg.  And  moreover,  from  paralysis 
of  the  muscles  which  rotate  the  head  and  eyes  to  the  opposite  side, 
the  patient  has  "  conjugate  deviation "  of  the  head  and  eyes 
towards  the  side  of  the  lesion,  owing  to  unopposed  action  of  the 
muscles  supphed  by  the  intact  hemisphere. 

If,  on  the  other  hand,  the  capsular  lesion  be  farther  back  along 
the  posterior  limb  of  the  capsule,  the  hemiplegia  will  afiect  the  leg 
much  more  than  the  arm,  and  the  face^only  shghtly  ;  whilst,  owing 
to  interference  with  the  sensory  tract,  which  lies  between  the  motor 
and  the  visual  fibres,  there  will  now  be  hemiansesthesia  also. 

Lastly,  if  the  lesion  be  at  the  extreme  posterior  end  of 
the  capsule,  there  will  be  not  only  hemiansesthesia  but  also 
hemianopia  from  interruption  of  the  visual  fibres.  Here  again 
we  note  that  it  is  impossible  for  a  single  capsular  lesion  to  produce 


10 


NERVOUS   DISEASES 


at  the  same  time  hemiplegia  and  hemianopia  without  also  pro- 
ducing hemiansesthesia. 

A  lesion  of  the  cms  cerebri  will  tend  to  implicate  the  third  cranial 
nerve  on  the  side  of  the  lesion,  producing  at  the  same  time  a  hemi- 
plegia of  face,  arm,  and  leg  on  the  opposite  side.  This  so-called 
"  Weber's  syndrome  "  is  one  variety  of  "  crossed  paralysis." 


Fig.  8. — Diagram  of  Tracts  in  the  Spinal  Cord. 


1.  Crossed    pyramidal  tract  (descending) 

and  Splno-thalamic  tract  (ascending). 

2.  Direct  pyramidal  tract. 

3.  Postero-internal  tract  (GoU). 

4.  Postero-external  tract  (Burdach). 


5.  Direct  or  dorsal  cerebellar  tract. 

6.  Ventral  cerebellar  tract  (Gowers). 

7.  Lissauer's  marginal  zone. 

8.  Lateral  ground-bundle. 

9.  Anterior  ground-bundle. 


A  unilateral  lesion  of  the  'pons  at  the  level  of  exit  of  the  facial 
nerve  will  produce  another  "  crossed  paralysis,"  viz.  : — facial  palsy 
on  the  side  of  the  lesion  with  hemiplegia  of  the  arm  and  leg  of  the 
opposite  side.  And  if  at  the  same  time  the  nucleus  of  the  sixth 
cranial  nerve  be  implicated  (which  is  not  unusual,  since  the  facial 
nerve  hooks  round  the  sixth  nucleus  within  the  pons),  we  have 
nuclear  palsy  of  the  sixth  nerve,  facial  palsy  on  the  same  side, 


ANATOMY    AND    PHYSIOLOGY  11 

and  hemiplegia  of  the  arm  and  leg  on  the  opposite  side  : — the 
"  Millard-Gubler  syndrome." 

Unilateral  lesions  of  the  fans  or  medulla  helow  the  level  of  the 
facial  nerve  leave  the  face  unafJected  and  produce  only  a  hemiplegia 
of  arm  and  leg.  And  a  unilateral  lesion  of  the  spinal  cord  below  the 
cervical  enlargement  will  produce  a  monoplegia  of  the  leg  on  the 
side  of  the  lesion  without  affection  of  the  arm.  It  will  also  produce 
some  anaesthesia  of  the  opposite  leg..  Such  motor  paralysis  of  one 
leg  and  sensory  paralysis  of  the  other  is  called  "  Brown-Sequard 
paralysis,"  to  which  we  shall  return  later  (p.  19). 

Fig.  8  is  a  diagram  representing  the  tracts  in  the  spinal  cord 
of  chief  clinical  interest.  There  are  also  other  ascending  and 
descending  tracts  of  minor  importance,  which  we  have  omitted 
from  the  diagram  for  the  sake  of  simphcity. 

The  pyramidal  tracts  are  by  far  the  most  important  descending 
tracts  in  the  cord,  for  they  convey  voluntary  motor  impulses  down- 
wards from  the  motor  cortex  towards  the  anterior  cornua.  The 
pyramidal  fibre  does  not  actually  join  the  anterior  cornu,  but  ends  in 
the  region  of  the  posterior  cornu,  whence  a  short  intermediate  con- 
necting-cell and  fibre  run  forward,  linking  it  to  the  anterior  cornual 
cell  (see  "Fig.  2).  Most  of  the  voluntary  motor  impulses  decussate 
at  the -lower  end  of  the  medulla  and  traverse  the  crossed  pjrramidal 
tract  in  the  lateral  column  ;  a  few  run  in  the  direct  pyramidal  tract 
and  cross  over  later  within  the  cord  itself.  A  few  pyramidal  fibres 
also  run  down  in  the  ipso-lateral  pyramidal  tract  (which  we  might, 
somewhat  paradoxically,  call  the  uncrossed  crossed-pyramidal  tract). 
These  fibres  probably  do  not  cross  over,  but  supply  motor  impulses 
to  the  ipso-lateral  leg.  They  account  for  the  occurrence  in  hemi- 
plegia of  certain  phenomena  on  the  opposite,  "  non-paralysed " 
side,  such  as  paresis,  increased  deep  reflexes,  and  sometimes  con- 
tractures in  the  "  healthy  "  lower  Hmb. 

In  addition  to  the  great  pyramidal  or  cortico-spinal  tracts,  there 
are  other  minor  tracts  which  enter  the  spinal  cord  from  above. 
These  are  derived  from  sub-cortical  centres,  and  constitute  sub- 
sidiary subcortico-spinal  tracts.  They  end  among  the  cells  of  the 
anterior  horns,  and  provide  a  mechanism  for  the  performance  of 


12 


NERVOUS   DISEASES 


N.CaoAat 


A  =  Crossed  pyramidal  tract. 
B  =  Direct 

1  =  Rubro-spinal  tract  ( ) 

2=Tecto-spiiial  tract   ( ) 

3= Vestibulo-spinal  tract  (...■) 

f.l.p-Fasciculns  longitudinalis 
posterior. 

f.l.v= Fasciculus  longitudinalis 
ventralis. 

lem  =  Fillet  or  lemniscus. 


3i 


C£US  CEREBRI 


P0^Y5 


MEDULLA 


SPIRAL  CORD 


Fig.  9.— Cortico-spinal  and  sub-cortico-spinal  tracts. 


ANATOMY    AND    PHYSIOLOGY  13 

certain  automatic  acts  which  may  still  be  possible  when  voluntary- 
motor  power  is  lost,  as  in  pyramidal  disease.  Of  these,  the  most 
important  are  the  following  (see  Fig.  9) : — 

1.  The  ruhro-S'pinal  or  fre-pyramidal  tract  (Monakow's  bundle). 
— This  tract  arises  in  the  red  nucleus  of  the  crus  cerebri,  decussates 
almost  at  once  in  the  tegmentum,  and  descends  in  the  contra-lateral 
side  of  the  pons  and  medulla  to  the  lateral  column  of  the  spinal  cord, 
where  it  Ues  ventral  to  the  crossed  pyramidal  tract. 

2.  The  tedo-spinal  tract  or  ventral  longitudinal  bundle. — This 
arises  in  the  mid-brain  from  the  anterior  corpus  quadrigeminum, 
crosses  over  in  Meynert's  "  fountain  "  decussation  beneath  the 
Sylvian  aqueduct,  and  then  runs  down  the  contra -lateral  side  of 
the  formatio  reticularis  to  the  ventral  column  of  the  spinal  cord. 

3.  The  vestibulospinal  tract  or  dorsal  longitudinal  bundle. — This 
arises  from  the  accessory  vestibular  nucleus  of  Deiters  within  the 
pons,  and  passing  downwards  mainly  on  the  ipso -lateral  side  of  the 
spinal  cord  in  the  ventral  column,  ends  amongst  the  anterior  cornual 
cells. 

In  the  adult  the  ventral  and  dorsal  longitudinal  bundles  are 
indistinguishable  from  each  other  on  section  of  the  meduUa  or 
spinal  cord,  but  they  myelinate  at  different  periods  of  development, 
and  can  thus  readily  be  differentiated  in  the  foetus. 

4.  The  fonto-S'pinal  tract. — This  is  derived  from  cells  of  the 
formatio  reticularis  of  the  pons.  Part  of  it  runs  down  the  ventral 
column  of  the  ipso -lateral  side,  whilst  part  decussates  in  the  raphe  of 
the  medulla  and  enters  the  opposite  lateral  column  of  the  spinal  cord. 

Sensory  Paths. — According  to  Head,  Eivers,  and  Sherren,^ 
the  various  afferent  impulses  from  the  periphery,  on  their  way 
towards  the  spinal  cord,  do  not  run  indiscriminately  along  the 
afferent  nerves  but  are  conducted  along  several  distinct  classes  of 
nerve  fibres.  According  to  these  observers,  common  sensation  is 
a  complex  affair,  based  on  three  kinds  of  sensibility  : — 

1.  Dee-p  sensibility,  a  variety  which  takes  cognisance  of  deep 
pressure,  and  which,  if  that  pressure  be  excessive,  is  capable 
of  producing  a  sensation  of  pain — ■''  pressure -pain."  Deep  sensi- 
1  Brain,  1905,  pp.  99-115. 


14 


NERVOUS   DISEASES 


bility  also  includes  sensations  from  muscles,  from  joints,  and 
the  vibration-sense  (see  later,  p.  195).  The  fibres  conducting  deep 
sensibility  run  along  with  the  muscular  nerves  and  are  not  de- 
stroyed by  division  of  all  the  sensory  nerves  to  the  skin. 

2.  Proto'pathic  cutaneous  sensibility,  a  variety  which  responds 


-l^yramidLalTroLct/ 


Sense  oFAcdve  MnscuXar  CanbrouctJMW. 

JotnJb  Sense. 

—  Temperalvre  ctndb  Tairv 

-ToLctile  Sense. 


Fig.  10. — Diagram  illustrating  the  course  of  the  various  sensory  paths  in 
the  spinal  cord. 

to  painful  cutaneous  stimuli  (pricking,  faradic  stimulation),  also  to 
extremes  of  cold  and  heat,  like  freezing  and  burning  (temperatures 
of  45°  C:  and  over,  and  of  10°  0.  and  under).  These  protopathic 
fibres  from  the  skin  are  the  first  to  regenerate  after  injury  to  a 
cutaneous  nerve,  so  that  the  protopathic  sensations  are  the  earliest 
to  recover  as  a  cutaneous  nerve  heals. 


ANATOMY    AND    PHYSIOLOGY  15 

3.  Epicritic  cutaneous  sensibility,  whose  fibres  are  the  slowest 
to  recover  after  injury.  This  group  includes  the  appreciation  of 
light  touches,  of  cutaneous  localisation,  the  recognition  of  finer 
differences  of  temperature — not  merely  between  hot  and  cold, 
but  between  warm  and  cool. 

These  differences,  it  should  be  noted,  apply  only  to  the  extra- 
spinal  portion  of  the  sensory  paths,  i.e.  to  the  peripheral  nerves. 

All  the  sensory  impulses,  whether  conveying  sensations  of 
touch,  temperature,  or  pain  from  the  skin,  sensation  of  active 
muscular  contraction  from  the  muscles  (kinsesthetic  sense),  or 
sensations  from  the  joints  or  bones,  enter  the  spinal  cord  through 
the  posterior  roots,  as  indicated  in  Fig.  10. 

Once  the  afferent  impulses  enter  the  spinal  cord,  it  is  no  longer 
a  question  of  deep,  epicritic,  or  protopathic  sensation  ;  they  now 
become  redistributed  in  simpler  fashion.  Thus  all  sensations  of 
temperature  run  together  in  one  tract,  whether  they  reached  the 
cord  by  the  protopathic  or  the  epicritic  route  :  similarly  all  sen- 
sations of  pain  run  together  in  the  cord,  whether  they  were 
protopathic  or  "  deep  "  in  the  peripheral  nerves,  and  so  on.  This  is 
indicated  in  the  following  scheme  : — 

Paths  in  Spinal  Coed.  Paths  in  Peripheral  Nerves. 


il 


Deep     .    .      a  Pressure. 


Posterior  Column  1  rp^.,  J /3  /  ^  Light  Touches. 

Lateral  Column     /  ^^'-"^"'5  \y  \y  Localisation. 

\S  Epicritic   .   ',  S  Differences  in  Size. 

/To,Tnr.<>r.o(->ivo/^  U  Moderate  differencss  of  Temperaturc. 

lemperature  ^  ^  ,^  Extreme  differences  of  Temperature. 

Lateral  Column    -|  ,  Protopathic |  ^  cutaneous  Pain  (pricks,  freezing,  burns. 


i. 


f 


electricity). 
9  Pressure-Pain. 


/  Muscles  t     Deei)  J  '  Lengthening  or  Shortening  of  Muscles. 

Posterior  Column-'  Joints  k  k  .Joints — passive  movements. 

U  Vi): 


Deep 
L(Bonet"  ^  ^^  Vibration  (tuning-fork). 


Of  these  various  impulses,  the  fibres  conveying  sensations 
from  the  muscles  and  joints,  together  with  the  smaller  part  of  the 
fibres  for  tactile  sensation,  ascend  in  the  posterior  colunm.  to  the 
gracile  and  cuneate  nuclei  of  the  same  side  of  the  medulla.  Most 
of  the  fibres  for  tactile  sense,  together  with  those  for  temperature 
and  pain,  cross  in  the  anterior  commissure  to  the  opposite  side 


16  NEEVOUS    DISEASES 

(these  crossed  fibres  not  coming  directly  from  the  posterior  root, 
but  through  the  relay  of  another  cell  in  the  posterior  horn)  and 
ascend  the  cord  in  the  opposite  lateral  column,  in  the  spino- 
thalamic tract.  Thus  the  lateral  column  conducts  not  only 
pyramidal  motor  impulses  coming  down,  but  also  spino -thalamic 
ascending  im.pulses  of  touch,  temperature,  and  pain. 

The  upward  course  of  the.  various  sensory  fibres  through  the 
medulla  and  pons  is  somewhat  complicated,  and  not  yet  entirely 
settled,  but  the  most  probable  arrangement  is  shown  in  Fig.  11. 

Most  of  the  fibres  for  touch  cross  the  middle  line  in  the  spinal 
cord,  as  already  explained,  and  then  pass  directly  upwards  in  the 
spino-thalamic  tract  of  the  lateral  column  and  into  that  part  of  the 
medulla  called  the  formatio  reticularis.  The  formatio  reticularis 
leads  the  fibres  up  through  the  pons  and  crus  to  the  optic  thalamus, 
and  thence  they  pass  through  the  posterior  limb  of  the  internal 
capsule  to  the  sensory  cortex  behind  the  fissure  of  Eolando. 

As  the  sensory  tract  traverses  the  pons  it  passes  along  the 
inner  side  of  the  sensory  spinal  root  of  the  trigeminal  nerve  of  the 
same  side.  Thus  a  unilateral  lesion  of  the  formatio  reticularis 
just  below  the  exit  of  the  fifth  or  trigeminal  nerve  will  produce  a 
"  crossed  ansesthesia,"  i.e.  anaesthesia  of  the  face  on  the  side  of 
the  lesion,  and  of  the  arm,  leg,  and  trunk  of  the  opposite  side.  But 
higher  up  the  pons  the  sensory  fibres  from  the  face  also  cross  the 
middle  line,  so  that  a  lesion  of  the  formatio  reticularis  in  the  crus 
cerebri  will  now  cause  complete  hemiansesthesia  of  face,  arm,  and 
leg  (see  Fig.  12). 

The  fibres  for  temperature  and  pain,  entering  by  the 
posterior  root,  pass  into  the  grey  matter  of  the  posterior  cornu. 
There  they  start  afresh  and  cross  to  the  opposite  side  of  the 
cord,  ascending  in  the  opposite  lateral  column  near  the  crossed 
tactile  fibres.  On  reaching  the  medulla,  they  diverge  "from  the 
tactile  fibres  and  pass  to  the  outer  side  of  the  olivary  body,  close 
to  the  lateral  margin  of  the  medulla  and  intermingled  with  the 
fibres  of  Gowers'  tract.  They  then  leave  the  region  of  Gowers' 
tract  and  pass  upwards  through  the  pons,  gradually  inclining  to- 
wards the  other  sensory  tracts  and  ultimately  ascending  with  them 


ANATOMY   AND    PHYSIOLOGY 

_L 


17 


CcLUjoLodeNiLclews 
Optix:  ThxtLcoTuis 


FornuxUoReticularis 
Taiet 


CorpiusResUforme 
V  ITerve, 


Fibres  of  SpinalRoot  ofV  — 


Corpus  JlesU^orme-  - 

FornuxtioEMicuJjzris  - 

SpxjwCbRoct  of  V 

Fart  cf  Cowers  TrouU. — 
TiJLet--i 

/ 
/ 

JNiwIeius  Gracilis  ■ 
NvucLeubs  Cuneaius- 

SpinaLRoot  of  V 

Direct  Cerebellar Draxt 

Part  of  Gowers'TroMb 

FOUL  - 


Tax:tiJ^  Sense  [Uncrossed/) 
Joint  Sense  cLo. 

Kiruojesthetic  Sense         do 

PosterLorRcob 1 


FONS 
Level  of  V Nerve. 


-I  entlcuLarNmileas 


FONS 
level  of  8"^ Nerve. 


EauihJbriujn.' 
(Direct  CereheUoir  Troucb) 


MEDULLA 
FormoUijo  RelicuJxiris. 


-  Tficfile  Sense  (Crossed) 
-  -i Temperature  &Pain,  (Crcissed) 

E(^  uiUbriiun,    (Uhcrossed  } 

SPINAL  CORD 


Fig.  1  ]  .—Diagram  of  Chief  Sensory  Tracts  in  Spinal  Cord,  Medulla, 
Pons,  and  Cerebrum. 


18 


NERVOUS   DISEASES 


to  the  optic  thalamus  and  thence  through  the  internal  capsule  to 
the  cortex.  Gowers'  tract,  now  separate  from  the  temperature 
and  pain  fibres  in  the  upper   part    of   the   pons,  hooks  sharply 


VITerve 


Letf. 

Fig.  12. — Course  of  Sensory  Fibres  in  the  Pons  (Starr). 

A.  Lesion  causing  right  heniiansesthesia. 

B.  Lesion  causing  "  alternate  hemianEesthesia  "  of  left  face  and  right  side  of  body. 

backwards    and    enters  the  cerebellum  from  above,   through  the 
superior  peduncle. 

The  sensory  fibres  from  muscles  and  from  hones,  together  with 
the  uncrossed  minority  of  tactile  fibres,  ascend  uncrossed  in  the 
posterior  column  of  the  cord  to  the  nucleus  gracilis  and  nucleus 
cuneatus,  the  nucleus  gracihs  receiving  the  fibres  from  the  lower 
limb,  the  nucleus  cuneatus  those  from  the  upper  limb.  From  these 
two  nuclei,    nerve   fibres  pass  upwards,    and    cross    the    middle 


ANATOMY    AND    PHYSIOLOGY  19 

line  in  the  internal  arcuate  fibres,  forming  the  superior  sensory 
decussation  of  the  fillet  (contrast  this  with  the  spinal  decussation 
of  the  thermal,  pain,  and  the  majority  of  the  tactile  fibres).  The 
sensory  fibres  from  the  leg,  passing  through  the  nucleus  gracilis, 
cross  lower  down  than  those  from  the  arm,  which  go  through  the 
nucleus  cuneatus.  Having  crossed  to  the  opposite  side  and  reached 
the  fillet,  a  flattened  strand  of  fibres,  they  pass  upwards  in  that 
tract  not  far  from  the  thermal  and  pain  fibres.  The  main  mass 
of  the  tactile  fibres  ascends  through  the  crus  cerebri  to  the  optic 
thalamus,  and  passes  on  through  the  internal  capsule  to  the  sensory 
cortex,  which  lies  mainly  behind  the  Rolandic  fissure,^  and  partly 
also  in  the  gyrus  fornicatus,  on  the  mesial  aspect  of  the  brain. 

We  have  still  to  consider  another  tract,  which  conducts  sensory 
fibres  for  the  sense  of  equilibrium.  This  tract  does  not  commence  in 
the  posterior  root-ganglion  but  arises  as  an  "  endogenous  "  tract 
within  the  cord.  Arising  from  the  cells  of  Clarke's  column  at  the 
base  of  the  posterior  horn,  it  constitutes  the  direct  cerebellar  tract 
and  ascends,  uncrossed,  into  the  restiform  body  and  cerebellum. 

Before  leaving  the  motor  and  sensory  tracts  within  the  central 
nervous  system  it  will  be  useful  to  mention  the  symptoms  produced 
by  a  lesion  of  one  lateral  half  of  the  spinal  cord.  Such  a  lesion 
is  most  commonly  the  result  of  a  stab  in  the  back ;  less  commonly  it 
is  produced  by  bullet-wounds,  fractured  spine,  caries,  or  by  chronic 
diseases  of  the  spinal  cord  itself.  The  syndrome  which  results  is 
known  as  Brown-Sdquard  paralysis,  and  it  will  be  readily  understood 
by  reference  to  Figs.  10  and  13.     The  symptoms  are  as  follows  : — 

(1)  On  the  side  of  the  lesion  we  have,  from  interruption  of  the 

^  Sensory  impulses  run  up  not  only  to  the  post-central  convolutions,  but 
also  to  the  motor  areas.  Thus  a  lesion  of  the  motor  cortex,  besides  causing 
a  monoplegia  of  the  corresponding  limb,  produces  slight  anaesthesia  of  the 
affected  limb,  with  deficient  sense  of  position  in  the  weakened  parts  and 
diminished  kingesthetic  sense  in  the  affected  muscles.  It  is  to  be  borne  in 
mind  that  the  pyramidal  motor  cells  do  not  lie  in  the  most  superficial  layer 
of  the  cortex,  but  are  covered  by  a  layer  of  cells  which  are  probably 
sensory  in  function.  A  striking  evidence  of  this  was  afforded  by  a  case 
of  Negro  and  Oliva.  These  observers  had  the  opportunity  of  stimulating 
the  motor  cortex  of  a  woman  who  had  been  trephined.  They  found  that 
with  feeble  stimulation  only  sensory  symptoms  were  produced,  a  stronger 
stimvilus  being  required  to  cause  motor  spasms. 


20 


NERVOUS   DISEASES 


motor  tract,  motor  paralysis  of  the  corresponding  leg,  witli  an 
extensor  plantar  reflex  from  tlie  outset  and,  later  on,  exaggeration 
of  the  deep  reflexes.     There  is  a  slight  and  transient  elevation  of 


SIDE  OF  LESION 


Loss  or  SenxsaJtiorv  irv  Joints 
anob  Mvbscles. 

.CutaneoasTh£rni-Anaesthesia- 

ajhdb  Anolgesixx,. 
FartLoL  CvJtxxjieoUjsIoucdLsArmjssttussiji, 

Motor  PoLrah/sis. 

Vaso-mxjtorFaraJysis. 

Loss  of  Vibratiani-sense  inBones. 

Cutauteou^  JfyperaesOiesia,. 


Fig.  13. — Diagram  illustrating  the  symptoms  resulting  from  a  left-sided 
hemi-section  of  the  spinal  cord  (Brown-Sequaid  syndrome). 


temperature,  owing  to  the  interruption  of  vaso-motor  fibres  which 
descend  in  the  lateral  column.  There  is  loss  of  sense  of  position 
on  passive  movement  of  the  limb  and  loss  of  "  vibration  sense  " 
(tested    by   a   tuning-fork)    in    the  bones   of  the   paralysed   leg, 


ANATOMY    AND    PHYSIOLOGY  21 

due  to  interruption  of  the  uncrossed  fibres  from  the  posterior 
roots  below  the  lesion,  which  ascend  in  the  posterior  cohimn. 
The  paralysed  leg  is  not  anaesthetic,  but,  just  at  the  level 
of  the  lesion,  there  is  around  the  trunk  a  narrow  zone  of 
anaesthesia  to  touch,  temperature,  and  pain,  from  severance 
of  a  few  sensory  fibres  cut  across  before  they  have  succeeded 
in  crossing  to  the  other  side.  Finally,  there  is  a  narrow  zone 
of  hjrpersesthesia  above  the  anaesthetic  zone,  perhaps  due  to 
local  irritation  of  the  lowest  unsevered  posterior-root  fibres 
in  the  cord,  close  above  the  lesion ;  but  this  explanation  is  in 
dispute. 

(2)  On  the  side  opposite  to  the  lesion  there  is  no  motor  paralysis. 
But  there  is  loss  of  cutaneous  sensation  to  temperature  and  pain 
(completely),  and  to  touch  (partially),  in  the  non-paralysed  lower 
limb  and  in  the  corresponding  half  of  the  trunk  up  to  the  level  of 
the  lesion.  There  is  a  zone  of  hjrperaesthesia  above  the  anaes- 
thetic area,  as  on  the  side  of  the  injury.  Motor  power  is  unim- 
paired, so  also  is  the  sensation  of  position  on  active  or  passive 
movement  of  the  limb. 

Cerebellum. — The  cerebellum  consists  of  a  middle  lobe  or 
vermis,  with  a  lateral  lobe  on  each  side,  and  its  cortex  is 
finely  folded  into  leaves  or  lamellae.  Within  the  white  matter, 
at  a  distance  from  the  cortex  and  analogous  in  some  respects  to 
the  basal  gangha  of  the  cerebrum,  there  are  several  important 
masses  of  grey  matter,  of  which  the  chief  are  the  corpora  dentata, 
two  hollow  crumpled  sacs,  one  within  each  lateral  lobe ;  the  roof 
nuclei  within  the  middle  lobe ;  the  nuclei  glohosi  and  the  nuclei 
emholiformes,  bilaterally  situated,  between  the  roof  nucleus  and 
the  dentate  nucleus  (see  Fig.  14) ;  and  the  nuclei  of  Deiters,  or  acces- 
sory vestibular  nuclei,  within  the  pons,  one  on  each  lateral  aspect. 
Deiters'  nucleus  has  several  highly  important  connections,  with 
the  cerebellar  cortex,  with  the  ocular  nuclei  (third  and  sixth), 
and  with  the  anterior  cornual  cells  of  the  same  side  of  the 
cord,  through  the  vestibulo- spinal  tract.  This  centre  in  Deiters' 
nucleus,  with  its  various  connections,  is  probably  the  lower  reflex 
mechanism  whereby,  when  we  hear  a  sound,  the  head  and  eyes  are 


22  NERVOUS    DISEASES 

promptly  turned  towards  the  side  on  which  the  auditory  stimulus 
was  received. 

Each  lateral  lobe  has  three  peduncles  (Fig.  15).  Of  these, 
the  superior  peduncle  contains  fibres  which  are  chiefly  cerebello- 
fugal  and  are  derived  mainly  from  the  dentate  nucleus,  this 
nucleus  in  turn  being  connected  with  the  cerebellar  cortex. 
The  cerebello-fugal  fibres  of  the  superior  peduncle  pass  up  ventral 
to  the  corpora  quadrigemina,  cross  the  middle  line  and  reach  the 
red  nucleus  in  the  crus  cerebri  of  the  opposite  side.     Starting  again 

/Nucleus  Tecti 
,'  /Nucleus  Glotosufe 
,'  /    /Nucleus  EwiTooliformis 
Nucleus  Dentiil'as 


Fig.  14. — Horizontal  section  through  cerebellum. 

from  this  station,  fibres  run  forwards  along  the  anterior  limb  of 
the  internal  capsule,  and  pass  to  the  optic  thalamus  and  to  the 
cortex  of  the  frontal  lobe.  In  this  way  the  cerebellar  hemisphere 
of  one  side  is  connected  with  the  opposite  side  of  the  cerebrum,  such 
connection  being  not  a  direct  one,  from  cortex  to  cortex,  but  indirect, 
by  the  intermediation  of  intra-cerebellar  and  intra-cerebral  nuclei. 

The  middle  peduncle  constitutes  the  greater  part  of  the  trans- 
verse fibres  of  the  pons.  And  here  again  its  fibres  are  not  mere 
commissural  strands  running  from  one  lateral  lobe  to  the  other. 
Fibres  from  each  lateral  lobe  cross  the  middle  line,  it  is  true,  but 
they  end  in  cells  in  the  formatio  reticularis  of  the  opposite  side 


ANATOMY    AND    PHYSIOLOGY 


23 


of  the  pons.      There  new  fibres  arise  and  pass  up   the   superior 
peduncle  through  the   crus  cerebri  and  internal  capsule  to  the 


SPINAL   CORO 


Fig.  15. — Cerebello-petal  ( )  and  cerebello-fugal  (  —  - )  paths. 

frontal,  temporal,  and  occipital  lobes  of  the  cerebrum.  Im- 
portant afferent,  cerebello-petal  fibres  in  the  middle  peduncle 
connect  Deiters'  nucleus  with  the  vermis  and  the  corresponding  side 


24  NERVOUS    DISEASES 

of  the  cerebellar  cortex  in  the  region  of  the  flocculus,  conveying 
impulses  to  the  cerebellum  from  the  semicircular  canals. 

The  inferior  peduncle  or  restiform  body  connects  the  cere- 
bellum with  the  medulla  and  spinal  cord.  It  contains  the  direct 
cerebellar  tract,  conveying  impulses  of  equilibration  from  the 
same  side  of  the  spinal  cord,  also  arcuate  fibres  from  the  pos- 
terior column  nuclei  of  both  sides,  and  fibres  from  the  inferior 
olive  of  the  opposite  side.  All  these  fibres  are  cerebello-petal, 
leading  upwards. 

Broadly  speaking,  then,  each  lateral  half  of  the  cerebellum  is 
in  connection  mainly  with  the  cerebral  hemisphere  of  the  opposite 
or  contra-lateral  side,  with  both  sides  of  the  medulla,  and  with  the 
same  or  ipso-lateral  side  of  the  spinal  cord. 

Thus  the  cerebellum  receives  impulses  from  various  sources  : — 
from  the  cerebrum  through  the  superior  peduncles,  from  the  skin 
and  muscles  through  the  inferior  peduncles,  and  from  most  of  the 
cranial  nerve  nuclei  through  the  middle  peduncles,  especially  from 
the  semicircular  canals,  by  the  vestibular  nerve.  And  in  turn  the 
cerebellum  sends  efferent  impulses  to  the  cerebrum,  reinforcing 
the  general  muscular  tonus  and  co-ordinating  the  motor  impulses 
proceeding  from  the  cerebrum.  In  most  voluntary  movements  the 
centre  of  gravity  of  the  body  requires  to  be  altered  and  certain 
muscular  groups  have  to  co-ordinate  to  maintain  equilibrium. 
For  this  purpose  the  tonus  of  these  muscular  groups  has  to  be 
augmented,  and  this  is  accomplished  by  the  cerebellum,  the  great 
centre  for  co-ordination  and  equilibration,  partly  by  the  action  of 
the  dentate,  roof,  and  emboliform  nuclei  on  the  cerebral  motor 
cortex,  partly  by  the  nuclei  of  Deiters  and  the  descending  vestibulo- 
spinal tracts  to  the  spinal  cord. 

Experiments  ^  have  shown  that  although  the  cerebellum  as  a 
whole — comprising  cortex  and  nuclei — responds  to  stimulation, 
the  cerebellar  cortex,  compared  with  the  cerebral,  is  relatively 
very  resistant  to  excitation.  On  the  other  hand,  the  sub-cortical 
cerebellar  nuclei  are  highly  excitable,  and  it  is  probable  that 
stimulation  of  the  cerebellum  produces  motor  phenomena  mainly 
1  Horsley  and  Clark,  Brain,  1908,  p.  45.  L 


ANATOMY    AND    PHYSIOLOGY  25 

by  excitation  of  these  nuclei.  If  we  stimulate  one  lateral  lialf  of 
tlie  vermis  or  tlie  lateral  cerebellar  hemisphere,  we  produce  move- 
ments of  the  ipso-lateral  limbs  and  also  rotation  of  the  body 
around  its  own  longitudinal  spinal  axis.  Thus  excitation  of  the 
right  side  of  the  cerebellum  produces  a  rotation  in  the  direction 
of  unscrewing  an  ordinary  screw  (the  animal's  head  representing 
the  head  of  the  screw).  Conversely,  removal  or  division  of  the 
right  lateral  lobe  produces  rotation  in  the  reverse  direction — 
namely,  that  of  screvfing  in  a  screw — since  the  intact  side  of  the 
cerebellum  maintains  its  tonic  action,  and  is  no  longer  opposed 
by  the  affected  side  whose  muscles  have  lost  their  tonus  (hypotonia). 
In  such  unilateral  destructive  lesions  loss  of  co-ordinating  influence 
also  causes  asynergia  of  the  ipso-lateral  arm  and  leg,  together 
with  various  ocular  phenomena,  including  nystagmus,  owing  to 
loss  of  cerebellar  influence  on  the  ocular  nuclei  through  Deiters' 
nucleus. 

Stimulation  of  the  vermis  in  the  middle  line  produces  bilateral 
movements.  Thus,  if  the  posterior  end  of  the  vermis  be  stimu- 
lated, the  animal  rotates  violently  forwards,  whilst  if  the  anterior 
part  of  the  vermis  be  stimulated,  the  animal  rotates  violently  back- 
wards. Destruction  of  the  middle  lobe  produces  opposite  effects, 
the  animal  tending  to  fall  forwards  from  an  anterior  lesion  of  the 
vermis,  and  conversely. 

The  movements  of  the  trunk  and  limbs  which  result  from 
stimulation  of  the  cerebellar  cortex  are  apparently  not  produced 
by  direct  action  of  the  cerebellum  on  the  spinal  cord.  Not  only 
is  there  no  direct  tract  leading  downwards  from  the  cerebellum 
into  the  cord  but  only  indirect  paths  through  Deiters'  nucleus 
and  the  vestibulo-spinal  tract,  but  Pagano  ^  has  shown  that  if  the 
contra-lateral  cerebral  cortex  be  extirpated,  stimulation  of  the 
lateral  lobe  of  the  cerebellum  no  longer  induces  movements  in  the 
ipso-lateral  limbs.  The  motor  action  of  the  cerebellar  nuclei  is 
exercised  indirectly,  through  the  intermediation  of  the  superior 
peduncles  and  the  cerebral  cortex. 

The  pituitary  gland  is  a  small  oval  body  whose  longest  diameter 
^  Rivista  di  patologia  nervosa  e  mentale,  1902,  p.  145. 


26  NERVOUS    DISEASES 

lies  transversely.  It  occupies  the  sella  turcica  of  the  sphenoid  bone. 
It  is  enclosed  within  a  special  covering  of  dura  mater,  and  is  connected 
with  the  floor  of  the  third  ventricle  by  a  narrow,  hollow  stalk — the 
infundibulum,  which  leads  upwards  through  a  special  aperture  in 
the  dura.  The  pituitary  gland  consists  of  two  lobes  : — (1)  a 
larger  anterior  lobe,  purely  epitheUal  in  structure  and  containing 
many  chromophile  cells  of  active,  secreting  nature ;  (2)  a  smaller 
"posterior  lohe  which  is  subdivided  into  a  pars  intermedia,  epithehal 
in  structure,  but  without  chromophile  cells  and  a  pars  nervosa,  the 
continuation  of  the  infundibulum,  and  consisting  of  ependymal 
and  neuroghal  cells.  The  pars  nervosa  is  developed  by  outgrowth 
from  the  primitive  brain,  whereas  the  pars  intermedia  and  anterior 
lobe  are  developed  as  a  backward  diverticulum  from  the  primi- 
tive ectoderm  of  the  pharynx.  In  fact,  a  small  longitudinal  patch 
of  pituitary  tissue  often  persists  in  the  submucous  tissue  of  the 
pharyngeal  roof,  outside  the  cranial  cavity.-^  The  secretion  of  the 
anterior  lobe  enters  the  blood-stream  of  the  venous  sinuses  around 
the  gland,  whereas  the  secretion  of  the  pars  intermedia  and  pars 
nervosa  probably  passes  directly  between  the  ependymal  cells  into 
the  cerebro-spinal  fluid  of  the  third  ventricle,  and  thence  enters 
the  blood-stream,  via  the  dural  sinuses.  The  secretion  of  the  pars 
nervosa  has  a  marked  effect  in  raising  the  general  vascular  pressure. 

^  Civalleri,  Giornate  delV  Accademia  di  Torino,  1907. 
Haberfeld,  Ziegler's  Beitrdge  zilr  path.  Anat.,  1909,  xlvi. 


CHAPTER   II 

ANATOMY   AND   PHYSIOLOGY  {continued) 

Having  considered  the  chief  motor  and  sensory  tracts  within  the 
central  nervous  system,  let  us  now  pass  to  the  peripheral  paths 
whereby  the  central  nervous  system  is  connected  with  the  various 
end- organs. 

Firstly,  as  to  the  motor  system.  Motor  fibres  starting  in  the 
cortex,  and  passing  down  the  pyramidal  tract,  as  already  described, 
reach  the  nuclei  of  the  various  motor  cranial  nerves  in  the  crura, 
pons,  and  medulla.  Then,  passing  along  the  spinal  cord,  the 
pyramidal  tract  gives  off  fibres  to  the  anterior  cornua  at  various 
levels  all  the  way  down.  This  portion  of  the  motor  tract,  from  the 
motor  cortex  to  the  extremity  of  the  pyramidal  fibres,  is  called 
the  upper  motor  neurone,  and  if  the  cortical  motor  cell  or  its  axon, 
the  pyramidal  motor  fibre,  be  destroyed,  we  have  degeneration 
of  the  whole  length  of  the  pyramidal  fibre  below  the  level  of 
the  lesion,  stopping  short  when  it  reaches  the  anterior  cornual 
cell.  This  so-called  "  descending  degeneration  "  does  not,  as  the 
name  might  suggest,  begin  at  the  lesion  and  spread  downwards, 
but  affects  simultaneously  the  whole  motor  fibre  below  the  lesion, 
on  the  side  remote  from  the  nerve-cell  which  is  its  trophic  centre. 

From  each  anterior  cornual  cell  a  new  motor  fibre  passes  out 
of  the  cord  along  an  anterior  nerve-root,  enters  into  the  formation 
of  a  peripheral  motor  nerve,  and  thereby  is  conducted  to  a 
muscle-fibre.  This  lower  segment  of  the  motor  path,  starting  at 
the  anterior  cornual  cell  and  ending  in  the  muscle-fibre,  is  called 
the  lower  motor  neurone.  Here  also,  if  the  anterior  cornual  cell  or 
its  axon,  the  peripheral  motor  nerve,  be  destroyed,  we  again  have 
a  "  descending  degeneration  "  of  the  whole  fibre  on  the  distal  side 
of  the  point  of  injury,  and  of  the  muscle-fibre  also.  We  note  that 
degeneration  of  the  upper  motor  neurone  does  not  spread  into  the 
lower  neurone,  nor  vice  versa.     It  is  particularly  to  be  remembered 


28  NEEVOUS    DISEASES 

tliat  a  lesion  of  the  upper  motor  neurone  leaves  the  lower  reflex 
arc  intact,  whilst  a  lesion  of  the  lower  motor  neurone  not  only 
severs  the  reflex  arc,  but  also  causes  the  muscle-fibre  in  that  reflex 
arc  to  degenerate  and  waste  away. 

Therefore  in  diagnosing  the  position  of  the  lesion,  in  any  given 
case  of  motor  paralysis  due  to  organic  disease,  the  first  question 
we  must  ask  ourselves  is  whether  the  lesion  is  in  the  upper  (cortico- 
spinal) or  in  the  lower  (spino-muscular)  motor  neurone.  There 
is  usually  little  difficulty  in  answering  this  question,  if  we  bear  the 
following  points  in  mind  : — 

Lesion  of  Upper  (Cortico-Spinal)      Lesion  of  Lower  (Spino-muscular) 
Motor  Neurone.  Motor  Neurone. 

1.  Motor  Paralysis.  1.  Motor  Paralysis. 

2.  Spasticity.  2.  Flaccidity. 

3.  No     muscular    wasting    (apart  3.  Muscular  Atrophy. 

from  disuse). 

4.  Electrical  reactions  normal.  4.  R.D.  (reactions  of  degeneration). 

5.  Deep  reflexes  present  and  often  5.  Deep  reflexes  absent  or  dimi- 

increased.  nished. 

6.  Extensor  plantar   reflex  (if  leg  6.  Plantar    reflex,    if    present,    of 

aff'ected).  normal  flexor  type  (unless 

lesion       paralyses       flexor 
muscles  themselves). 

Having  thus  recognised  which  motor  neurone,  upper  or  lower,  is 
affected,  we  have  then  to  decide  at  what  level  in  the  affected  neurone 
the  lesion  is  situated.     To  that  point  we  shall  come  later  (p.  215). 

Returning  for  a  moment  to  the  sensory  fibres ;  these  may 
also  be  regarded  as  arranged  in  sensory  neurones.  The  lowest 
sensory  neurone  starts  from  a  sensory  end-organ,  in  the  skin  or 
elsewhere,  and  extends  up  to  the  nerve-cell  in  the  intervertebral 
ganglion  on  the  posterior  spinal  root.  This  ganglion-cell  is  the 
trophic  centre  for  the  peripheral  sensory  fibre,  and  a  lesion  at  or 
below  this  cell  will  cause  "  descending  degeneration  "  of  the  distal 
segment  of  the  fibre  and  of  the  peripheral  end-organ.  There  is, 
however,  one  sensory  end-organ,  the  muscle-spindle,  which  is  an 
exception  to  this  rule,  and  does  not  degenerate  when  the  afferent 
fibre  leading  from  it  to  the  ganglion-cell  is  destroyed.  The 
mascle-spindle  thus  has  its  trophic  centre  within  itself. 

But  the  ganglion-cell  of  the  posterior  root  is  also  the  trophic 
centre  for  the  fibre  which  passes  upwards  from  it  along  the  pos- 


ANATOMY    AND    PHYSIOLOGY  29 

terior  root  and  enters  the  posterior  column  of  the  spinal  cord. 
And  therefore  a  lesion  at  or  above  the  intervertebral  ganglion-cell, 
in  the  posterior  root,  or  in  its  intra-spinal  prolongation  in  the  pos- 
terior column,  will  cause  an  "  ascending  degeneration  "  of  the  fibre 
through  its  whole  course  within  the  spinal  cord.  Here  again  this  so- 
called  "  ascending  "  degeneration  occurs  simultaneously  throughout 
the  entire  extent  of  the  nerve-fibre,  on  the  side  remote  from  its 
trophic  centre  in  the  intervertebral  ganglion  ;  and  this  degeneration 
extends  as  far  as,  but  does  not  imphcate,  the  next  nerve-cell  whose 
axon  leads  upwards  towards  the  brain.  Similarly  a  lesion  of  this 
second  sensory  neurone  causes  ascending  degeneration  in  the  fibre 
of  the  fillet  above,  as  far  as,  but  not  including,  the  optic  thalamus. 
There  a  third  neurone  starts,  leading  up  to  the  sensory  area  of  the 
cerebral  cortex.  In  the  case  of  the  ordinary  sensory  tract,  the 
path  traverses  the  internal  capsule. 

In  the  case  of  an  impulse  which  traverses  the  cerebellum, 
the  chain  of  successive  neurones  is  more  complex,  and  consists, 
firstly  of  a  posterior-root  neurone,  secondly  of  an  ascending 
spino-cerebellar  neurone,  thirdly  of  a  cerebello-dentate,  fourthly 
of  a  dentato-thalamic,  and  lastly  of  a  thalamo-cortical  neurone. 

The  so-called  "  Wallerian  degeneration  " — "  ascending  "  or 
"  descending  "  as  the  case  may  be — signifies  that  a  nerve-fibre, 
separated  from  its  trophic  cell,  degenerates  on  the  side  remote 
from  that  cell.  It  should  also  be  remembered  that  after  lesions 
of  a  cranial  or  spinal  nerve,  especially  in  a  young  animal,  marked 
chromatolytic  changes  are  produced  in  the  nerve  cells  of  the 
corresponding  motor  nucleus  in  the  bulb  or  spinal  cord. 

The  anterior  and  posterior  nerve-roots  join  to  form  mixed 
nerve-trunks.  These  again  branch  and  intermingle  to  form  plexuses 
in  the  cervical,  lumbar,  and  sacral  regions.  The  distribution 
of  the  difierent  nerves,  motor  and  sensory,  is  represented  in 
Figs.  16,  17,  and  18. 

Root  Lesions. — But  what  is  perhaps  less  familiar,  though  of 
equal  diagnostic  importance,  is  the  distribution  of  the  anterior 
and  posterior  spinal  roots.  In  lesions  of  the  lower  motor  neurone, 
we  have  often  to  decide  whether  the  distribution  of  symptoms 


30 


NERVOUS    DISEASES 


points  to  a  lesion  of  a  peripheral 
nerve-trunk,  such  as  the  musculo- 
spiral  or  sciatic,  or  whether  it 
points  to  a  lesion  of  one  or  more 
nerve-roots  before  they  have 
joined  to  form  the  trunks  of  a 
plexus.  Thus,  for  example,  the 
deltoid  is  frequently  paralysed 
alone  owing  to  a  lesion  of  the 
circumflex  nerve,  but  it  is  never 
paralysed  alone  as  a  result  of 
a  lesion  of  the  anterior  cornu  or 
anterior  nerve-root.  Again,  a 
lesion  of  the  musculo  -  spiral 
nerve  may  produce  paralysis 
both  of  the  supinator  longus 
and  of  the  extensors  of  the 
wrist  and  fingers,  but  these 
muscles  are  never  affected 
together  by  a  lesion  of  a 
single     segment      of      the      ,  | 


ea;  JSTJ  ut  3t^»/^ 


ANATOMY    AND    PHYSIOLOGY 


31 


spinal  cord  or  of  a  single  anterior  root,  since  their  motor  cells  lie 
at  difierent  levels  in  the  anterior  cornu.  This  will  be  readily 
seen  on  studying  the  tables  on  p.  34,  which    show    the   nuclear 


representation  of  muscles  in  the  anterior  cornua  at  various  levels 
of  the  spinal  cord.  For  clinical  purposes,  the  distribution  of  each 
anterior  root  may  bs  considered  the  same  as  that  of  the  spinal 
segment  from  which  it  arises. 

In  connection  with  the  root  distribution  of  sensory  and  motor 


32 


NERVOUS    DISEASES 


ANATOMY  AND  PHYSIOLOGY 


33 


fibres,  it  is  interesting  to  note  that  in  each  embryonic  segment  or 
metamere,  the  muscular  territory  (myotome)  of  the  segment  corre- 
sponds more  or  less  closely  with  the  cutaneous  distribution 
(dermatome)  and  with  a  zone  of  the  bony  skeleton  (sclerotome). 
In  the  trunk  this  segmental  or  metameric  arrangement  is  com- 
paratively easy  to  recognise,  especially  in  the  thorax,  and  even  in 
the  limbs,  though  more  complex,  a  similar  arrangement  can  be 
made  out.     Thus,  as  Bolk  has  shown,  in  the  limbs  there  is  for 


Fig.  19. — Transverse  section  through  upper  third  of  thigh. 
The  thick  black  line  indicates  the  boundary  between  the 
pre-axial  and  post-axial  regions  of  the  limb.  The  fine  black 
Unes  mark  the  segmental  distribution.     (After  Bolk.) 

every  spinal  segment  a  corresponding  dermatome,  myotome,  and 
sclerotome,  but  they  are  subdivided  into  a  pre-axial  and  a  post- 
axial  division  in  each  case  (see  Fig.  19). 

We  observe  that  comparatively  few  muscles  are  confined  to  a 
single  segment,  but  that  most  of  them  are  represented  in  two  or 
more  segments.  If,  therefore,  a  cord  lesion  be  limited  to  one 
segment,  it  will  cause  complete  paralysis  of  the  muscles  con- 
fined to  that  particular  segment  and  partial  paralysis  of  muscles 
whose  motor  nuclei  extend  up  or  down  into  other  segments.  This 
explains  the  apparent  irregularity  in  the  distribution  and  degree 
of  paralysis  in  certain  cases  of  infantile  paralysis  and  other  diseases 
of  th3  anterior  horns. 

c 


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Oih|o  -  hyoildeus 


Thy  ro-liyoi 


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capularis 


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Triceps  b 
Flexors 
Extensors 
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Pronato 


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MuscuLAK   Localisation 

IN 

Cervical   Enlargement 


i'octoralis 
(sternal) 

Latiss.  dorsi 
P  e  c  t  o  r 


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Flexors  and 

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L4 

L5 

SI 

S2 

S3 

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Quadr 

itusLuoi 
Creraas 

bornm 
ter 

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Ilia 

ens 

Tensor 

fascise 

;. 

Gl 

uteus     nied  ins 

w 

Gl 

nteus    mini  mus 

Qu 

adratusfemoris 
Geme.lli 
Gluteus    maxim 
Obturator     inte 

us 
rnus 

Pectin 

ens 

Addue 

tor  long  us 

G 

r  a  c  i  1  i 

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(Iductor  bre 

Sartor 

Obturator 

Quadriceps 

Add 

VIS 

ins 

externus 
extensor 
n  c  t  0  r  mag' 
S  e 

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b  r  a  n  0  s 
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antaris 

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Peronen  s  longus 

1^ 

Peron.  brev. 

Tibiali's  posticus 

Flex.  long,  digitorum 

Muscular   Localisation 

Flex.llong.  halluc. 

Extens.  brov.  digitor. 

Ab  ductor    hallu 

CIS 

H 

Flex.  brev.  bal 

lue. 

O 

Lumbo-Sacral   Cord 

Lumbric 
Inteross 

ales 
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pq 

Sphincter  An 

i  exter. 

Le 

vator 

Aui 

Perineal 

Muscles 

ANATOMY    AND   PHYSIOLOGY 


35 


Fig.  20.— Diagram  of  Cutaneous  Areas  of  Posterior  Roots.    (After  Collier  and 
Purves  Stewart.) 


Fig.  21. — Sacro-coccygeal  Eoot-areas. 


Similarly  in  a  case  of 
cutaneous  anaesthesia  it 
is  important  todistinguisli 
between  a  posterior-root 
lesion  and  a  lesion  of  a 
peripheral  nerve-trunk 
such  as  the  radial  or  ulnar. 
The  distribution  of  the 
posterior  nerve-root-s  is 
indicated  diagrammati- 
cally  in  Figs.  20  and  21. 


36 


NERVOUS    DISEASES 


Paths  of  Special  Senses. — Olfactory  Path. — The  olfactory 
nerves,  about  twenty  on  each  side,  arising  from  the  under  surface 
of  each  olfactory  bulb,  perforate  the  cribriform  plate  of  the 
ethmoid  bone  and  are  distributed  to  the  olfactory  region  of  the 
nasal  mucous  membrane  on  the  superior  turbinal  body  and  the 
corresponding  uppermost  part  of  the  nasal  septum.  The 
central  olfactory  tract  has  various  connections,  not  of  great 
clinical    importance,    leading    to    the     optic    thalamus     and     to 


Fig.  22. — Diagram  of  Connections  of  Olfactory  Nerves. 

other  sub-cortical  ganglia.  It  connects  the  olfactory  bulb 
with  the  cortical  centre  for  smell,  situated,  as  we  have  aheady 
seen,  in  the  uncinate  gyrus  at  the  tip  of  the  temporo-sphenoidal 
lobe  (Fig.  4).  The  olfactory  tract  does  not  traverse  the 
internal  capsule.  Each  olfactory  bulb  is  connected  not  only 
with  the  uncinate  gjrrus  of  the  same  side,  but  also,  through  the 
anterior  commissure,  with  that  of  the  opposite  side.  (See 
Fig.  22.) 

Visual  Path. — This  is   of  great  clinical  importance.      Starting 
from  the  retina,  the  visual  fibres  run  backwards  along  the  optic 


ANATOMY    AND    PHYSIOLOGY  37 

nerve.  At  the  optic  chiasma  there  is  a  partial  decussation,  so  that 
the  fibres  from  the  left  halves  of  both  retinae  (corresponding  to  the 
right  halves  of  the  visual  fields)  run  together  in  the  left  optic 
tract,  and  vice  versa.  The  central  visual  impulses,  from  each 
macula  lutea,  pass  into  both  optic  tracts.  The  fibres  of  each  optic 
tract  run  backwards,  winding  around  the  outer  side  of  the  crus 
cerebri,  to  the  primary  optic  centres,  viz.  : — the  posterior  part 
of  the  optic  thalamus,  the  external  geniculate  body,  and  the 
anterior  corpus  quadrigeminum. 

From  these  three  stations  new  fibres  arise,  forming  the  "  optic 
radiation,"  passing  through  the  internal  capsule  behind  the 
fibres  for  common  sensation  (Fig.  7)  and  so  reaching  the  cortical 
half-vision  centre.  This  centre,  mainly  on  the  mesial  aspect  of 
the  hemisphere,  is  divided  into  an  upper  and  a  lower  part  by 
the  calcarine  fissure  (Fig.  4).  Above  the  fissure  is  the  cuneate 
lobe,  below  it  is  the  lingual  gyrus.  The  half -vision  centre  also 
extends  on  to  the  convexity  of  the  occipital  lobe  at  its  posterior 
extremity  (Fig.  3).  The  calcarine  fissure  forms  a  boundary- 
line  between  the  cortical  representations  of  the  upper  and  lower 
quadrants  of  the  corresponding  half  of  the  visual  field.  Therefore 
a  lesion  of  the  left  occipital  lobe,  or  of  the  whole  of  the  left 
cuneus  and  lingual  gyrus,  or  of  the  fibres  of  the  left  optic  radiation, 
will  cause  a  right-sided  hemianopia  in  both  visual  fields ;  a  lesion 
of  the  left  cuneus,  i.e.  limited  to  the  part  above  the  calcarine 
fissure,  will  cause  blindness  of  the  right  loiver  quadrant  of  both 
visual  fields  ;  whilst  if  the  lesion  be  below  the  left  calcarine  fissure, 
in  the  lingual  gyrus,  it  will  produce  blindness  of  the  right  U'liper 
quadrant  of  both  fields.  These  are  varieties  of  "  quadrantic 
hemianopia." 

Besides  the  half-vision  centre,  there  is  a  higher  centre  on  the 
convex  surface  of  the  occipital  cortex,  where  a  lesion,  if  sufii- 
ciently  superficial  (so  as  to  miss  the  subjacent  optic  radiations), 
may  cause,  not  hemianopia,  but  what  is  called  "  crossed  ambly- 
opia." This  means  a  concentric  contraction  of  both  visual  fields, 
more  marked  in  the  eye  of  the  side  opposite  to  the  side  of  the 


38 


NERVOUS    DISEASES 


lesion.  Such  a  lesion  has  not  been  conclusively  demonstrated 
in  gross  organic  disease,  but  crossed  amblyopia  is  one  of  the  most 
frequent  symptoms  in  hysteria. 

CUNEUS 


Optic  Radiations 
Corpus  Callosvim 

Optic  Thalamus' 
Corp.  genie,  ext 


Optic  Tract 


Optic  Nerve 


Visual  Word  Centre 


Auditory  Word-Centre 


Vocal  Word-Centre 


Fig.  23.— Diagram  of  Visual  Paths  (after  Vialet). 

Lesion  at  1      produces  Blindness  of  one  eye. 
,,       at  2  „        Bi-teniporal  Hemianopia. 

„       ,,  3  and  3  ,,        Bi-nasal  Hemianopia. 

,,       „  4  ,,        R.  Hemianopia  with  Hemiopic  Pupil  Reaction. 

,,       „  5  ,,  „  with  Normal  Pupil  Reaction. 


„  7 


Crossed  Amblyopia. 
Word-Blindness. 


Finally,  in  right-handed  people    there  is  in  the  left  angular 
gyrus  a  centre  for  the  storage   of  visual  memories  of  written  and 


ANATOMY    AND    PHYSIOLOGY  39 

printed  speech.  If  this  centre  be  destroyed,  we  have  word-blind- 
ness, wliich  may  or  may  not  be  associated  with  right  hemianopia, 
according  as  the  subjacent  optic  radiations  are  affected  or  not. 
Fig.  23  indicates  diagrammatically  these  various  fibres  and  centres, 
and  also  shows  the  effects  upon  the  visual  fields  of  lesions  in  various 
parts  of  the  visual  path. 

Grustatory  Path. — The  course  of  the  taste-fibres  outside  the 
brain  is  somewhat  complex,  and  we  shall  study  it  again  later  when 
we  consider  the  cranial  nerves.  It  is  probable  that  some  of  the 
taste  impulses,  chiefly  those  from  the  front  of  the  tongue,  enter  the 
brain  through  the  sensory  root  of  the  fifth  cranial  nerve,  some 
through  the  glosso -pharyngeal  nerve,  and  some  through  the 
nervus  intermedius  or  sensory  root  of  the  facial.  The  cortical 
centre  for  taste  is  in  the  front  part  of  the  temporal  lobe,  close 
to  the  olfactory  centre  (Fig.  4).  The  intra-cerebral  course  of  the 
gustatory  fibres  is  not  definitely  settled,  but  it  is  probable  that 
they  do  not  traverse  the  internal  capsule. 

Auditory  Path. — This  is  of  some  practical  importance  (Fig.  24). 
Entering  the  medulla  in  the  cochlear  division  of  the  eighth  nerve, 
the  auditory  fibres  embrace  the  restiform  body,  some  passing 
along  its  inner  side  to  the  ventral  auditory  nucleus,  others 
passing  along  its  outer  side  to  the  dorsal  auditory  nucleus.  From 
these  two  nuclei  new  fibres  pass  upwards  towards  the  cortex. 
A  few  run  up  uncrossed  in  the  fillet  of  the  same  side,  but  most 
of  the  fibres  decussate  and  ascend  in  the  fillet  of  the  opposite 
side.  Some  end  in  the  posterior  corpus  quadrigeminum,  others 
go  on  to  the  corpus  geniculatum  mediale,  and  finally  the  bulk 
of  them,  passing  through  the  sub-lenticular  region  of  the  internal 
capsule  behind  the  sensory  fibres,  reach  the  cortical  auditory 
centre  in  the  superior  temporal  convolution  (Fig.  3),  and  in  the 
anterior  transverse  temporal  convolution  of  Heschl : — Flechsig's 
"  auditory  gyrus  "  ■^  (situated  on  the  upper  surface  of  the  temporal 
lobe,  at  the  bottom  of  the  Sylvian  fossa,  immediately  behind  the 
insula),  with  which  the  superior  temporal  is  continuous.  We  note 
that  each  cortical  centre  receives  auditory  messages  from  both 
^  Neurologisches  Centralblait,  1908,  p.  1. 


40 


NERVOUS    DISEASES 


ears,  though  more  extensively  from  the  ear  of  the  opposite  side, 
and  that  therefore  a  lesion  limited  to  one  temporal  lobe  will  not 
cause  deafness.  In  right-handed  people  there  is  a  specially 
differentiated  portion  of  the  left  auditory  centre  where  memories 
of  word-sounds  are  stored  up  (Fig.  3). 


TEMPORAL  CORTEX 


Corp,  Genical  «xt 
Corp.  GeTiicul.  ntcdia).^ 


Fig.  24. — Diagram  of  Connections  of  Cochlear  and  Vestibular  Nerves. 

A  certain  amount    of  clinical    evidence  ^    supports  the    view 

that    there    is    a    special    cortical    centre     associated  with    the 

sensations    of    hunger    and    thirst.      It  would  appear  to  be    in 

the  temporal  lobe,   at  or  near  the  olfactory  centre.  Abscesses, 

injuries     and    tumours    in    this     region    have     been  associated 

with  voracious  appetite  and   intense  thirst,  persisting  for  weeks 
or  months. 

^  Stephen  Paget,  Essays  for  Students,  1898. 


ANATOMY    AND    PHYSIOLOGY 


41 


Arteries  of  the  Brain.— Most  cases  of  acute  brain  disease 
which  we  meet  with  in  practice  are  the  direct  result  of  some 
vascular  disease,  e.g.  haemorrhage,  thrombosis,  or  embolism.  It 
is  therefore  important  to  understand  certain  facts  about  the 
cerebral  circulation. 

The  brain  is  supplied  by  two  pairs  of  arteries — ^the  internal 
carotids  and  the  vertebrals,  as  shown  in  Fig.  25.  The  two 
vertebral  arteries  join  to  form  the  basilar  artery  which  runs 
forwards  in  the  middle  line  along  the  front  of  the  pons,  supply - 


Anterior  cerebral 


Middle  cerebral 


Sylvian 


Posterior  cere- 
bral 


Lenticulo-optic 

Lenticulo-striate 
set  of  arteries 

Internal  carotid 


Basilar 


Vertebral 


Fig.  25. — Arteries  at  the  Base  of  the  Brain.     One,  the  lenticulo-striate,  is 
called  the  artery  of  cerebral  hjemorrhage.     (After  Dercum.) 


ing  perforating  branches  to  the  pons  and  arteries  to  the  cere- 
bellum. Between  the  crura  cerebri  the  basilar  divides  into 
the  two  posterior  cerebral  arteries,  each  of  which  winds  round 
the  outer  side  of  the  crus,  supplying  it  as  it  passes,  and  also 
giving  branches  to  the  optic  thalamus  and  the  corpora  quadri- 
gemina.  Finally  it  reaches  and  supphes  the  lower  part  of  the 
temporo-occipital  cortex  (Figs.  26  and  27).  Each  posterior  cerebral 
artery  sends  a  posterior  communicating  artery  forwards  to  join 
the  internal  carotid. 


42 


NERVOUS   DISEASES 


The  internal  carotid,  close  to  its  termination,  gives  off  an 
important  branch — the  anterior  choroid  artery,  which  passes 
backwards  to  enter  the  descending  horn  of  the  lateral  ventricle. 
The  area  supplied  by  the  anterior  choroid  (see  Figs.  26  and  27) 
includes  the  posterior  two -thirds  of  the  posterior  limb  of  the  in- 
ternal capsule,  part  of  the  choroid  plexus  of  the  lateral  ventricle, 
and  also  the  uncinate  gyrus  of  the  temporal  lobe.-^  Finally,  the 
internal  carotid  divides  into  three  main  branches  —  anterior 
cerebral,  middle  cerebral,  and  posterior  communicating.     The  two 


Area,  o/" 
A  ntsFLor  Cerehru,l 


Mvdd^ 


Cere' 


Posterior  Cerehtub 


JrecL  of 
lysterwr  Cerebral 


4  n  tenor  CsrebraL 


Anterior  Choroid,  traiu^v 
of  Interrval  Carottdy. 


-Middle  Cerebral 
Fig.  26. — Diagram  of  arterial  supply  of  cortex. 


anterior  cerebral  arteries  are  connected  by  the  short  anterior  com- 
municating artery,  thus  completing  the  "  circle  of  Willis."  The 
anterior  cerebral  artery  passes  forward,  and  then,  curving  round 
to  the  top  of  the  corpus  callosum,  turns  backwards,  parallel 
with  its  fellow  of  the  opposite  side,  between  the  mesial  surfaces  of 
the  two  hemispheres.  Most  of  the  mesial  surface  of  the  cerebral 
hemisphere,  as  far  back  as  the  parieto-occipital  fissure,  is  supplied 
by  the  anterior  cerebral  artery  (Figs.  26  and  27).     It  also  sends 


Bsevor,  Brain,  1907,  p.  403. 


ANATOMY    AND    PHYSIOLOGY 


43 


brandies  over  the  edge  of  the  hemisphere  to  its  convex  surface, 
supplying  the  anterior  and  mesial  part  of  the  frontal  lobe  and  a 
small  part  of  the  parietal  lobule.  And  at  the  beginning  of  its 
course,  it  sends  a  few  perforating  branches  inwards  to  the  caudate 
nucleus. 

The  middle  cerebral  artery,  or  arteria  fossce  Sylvii,  is  clinically 
the  most  important  of  the  three.  Its  main  trunk  passes  upwards 
and  outwards  along  the  Sylvian  fissure  to  the  surface  of  the  island 
of  Eeil,  where  it  divides  into  its  terminal  branches.     At  its  be- 


Anterior  Cerebral/ 


-Posterior  Cc 


Middle  CerebraL 
^interior  Choroid/ 


If  OS  tenor  CereiraZ 


Fig.  27. 


-Arterial  supply  of  basal  ganglia  and  cortex. 
(After  Beevor.) 


ginning  it  gives  off  numerous  basal  perforating  arteries,  which 
enter  the  anterior  perforated  space  and  ascend  to  the  caudate  and 
lenticular  nucleus  (which  together  constitute  the  corpus  striatum), 
also  to  the  optic  thalamus.  These  branches  are  called  lenticular, 
lenticulo -striate,  and  lenticulo-optic,  according  to  their  distribu- 
tion. All  these,  and  especially  one  of  the  lenticulo -striate  arteries, 
are  frequently  the  seat  of  cerebral  haemorrhage.  The  main  trunk 
of  the  middle  cerebral  runs  along  the  Sylvian  fissure,  where  it 
divides  into  four  terminal  branches  (Figs.  26  and  27).  One  goes 
to  Broca's  convolution   (the   third  inferior   frontal) ;   another  to 


44 


NERVOUS    DISEASES 


the  lower  two-thirds  of  the  pre-central  convolution  and  to  the 
adjacent  part  of  the  second  frontal  convolution  ;  another  to  the 
post-central  convolution  and  the  adjacent  superior  parietal  con- 
volution ;  and  a  fourth  to  the  supra -marginal  convolution,  the 
angular  convolution  and  the  upper  temporal  convolutions,  and 
so  to  the  tip  of  the  lobe  on  its  mesial  aspect. 

The  cortical  arteries  anastomose  with  one  another,  but  not  so 


AnJf.  Radjicular^ 
branches  frorrvA  ~'^-^ 
JnlercosUnl 
Artery. 


AnJ^ Spinal  Artay. 


■''A  hranches  From, 

\  Intercostnl  Artery. 
BrcmjdvtoAnJtertorMedianFLssure 


Fosterior 

SpinaL-Artxry 


~  ~Posteru)r 
SpuiaLJrtery. 


Fig.  28.- 


-Diagram  of  the  course  and  distribution  of  the  terminal  arteries  of 
the  spinal  cord.     (After  Van  Gehuchten.) 


the  perforating  basal  vessels.  They  are  "  terminal  "  arteries,  and 
do  not  anastomose  either  with  each  other  or  with  the  cortical 
vessels.  Therefore  if  a  basal  artery  becomes  blocked  by  throm- 
bosis or  embolism,  a  permanent  area  of  necrosis  results.  On  the 
other  hand,  the  blocking  of  a  cortical  artery  admits  of  a  more 
favourable  prognosis,  since  a  collateral  circulation  may  develop 
and  the  necrotic  process  be  arrested. 

The    cerebellum   is    supplied   by   the    anterior    cerebellar    and 
superior  cerebellar  arteries  from  the  basilar,  and  by  the  posterior 


ANATOMY    AND    PHYSIOLOGY  45 

cerebellar  arteries  from  the  vertebral.  The  posterior  inferior 
cerebellar  artery,  which  supplies  the  lateral  aspect  of  the  medvilla, 
is  of  some  clinical  importance  inasmuch  as  when  it  is  thrombosed 
the  resulting  area  of  destruction  (including  the  inferior  olive,  the 
restiform  body,  and  the  intervening  nuclei  of  the  vagus  and 
glosso -pharyngeal)  produces  a  characteristic  unilateral  bulbar 
syndrome  (see  later,  p.  262). 

The  spinal  cord  is  supplied  by  three  main  arteries,  one  anterior 
and  two  posterior,  running  on  the  surface  along  the  entire  extent 
of  the  cord.  The  anterior  spinal  artery  arises  from  one  or  other 
vertebral,  receiving  a  small  communicating  branch  from  the  oppo- 
site vertebral.  As  it  runs  down  the  front  of  the  cord,  it  is  reinforced 
by  a  series  of  smaller  vessels,  derived  from  the  intercostal  and 
lumbar  arteries,  which  enter  here  and  there  along  the  anterior 
roots.  The  anterior  spinal  artery  sends  numerous  branches  deeply 
along  the  pia  mater  lining  the  median  fissure,  dipping  alternately 
into  the  right  and  left  sides  of  the  fissure,  and  supplying  the 
grey  matter  of  the  cord.  The  two  posterior  spinal  arteries,  one 
on  each  side,  also  arise  from  the  vertebral  arteries  and  run 
downwards  on  the  back  of  the  cord,  close  to  the  posterior  roots, 
being  reinforced  by  small  branches  entering  here  and  there  along 
the  posterior  roots.  Fig.  28  shows  diagrammatically  the  position 
of  these  various  spinal  arteries,  and  it  should  be  observed  that  the 
grey  matter  and  the  white  receive  their  blood-supply  from  different 
vessels.  Moreover,  Uke  the  perforating  basal  arteries  of  the  brain, 
all  the  spinal  arteries,  once  they  have  penetrated  the  cord,  are 
terminal  arteries  and  do  not  anastomose.  Therefore  embolism  or 
thrombosis  of  a  spinal  artery  always  produces  an  area  of 
necrosis. 

The  Venous  Circulation  in  the  brain  is  pecuhar,  inasmuch  as  the 
direction  of  the  blood-stream  in  the  cortex  is  the  same  in  the 
arteries  as  in  the  veins,  i.e.  from  before  backwards.  The  superior 
longitudinal  sinus  receives  not  only  the  superior  cerebral  veins  from 
the  cortex,  but  also  some  veins  from  the  scalp,  and  through  its 
starting-point  at  the  foramen  csecum  it  receives  branches  from  the 
nasal  vein,  though  after  childhood  this   foramen   often  becomes 


46  NERVOUS    DISEASES 

closed.  Therefore  when  thrombosis  of  the  superior  longitudinal 
sinus  occurs  in  a  marasmic  child,  we  expect  epistaxis,  convulsions, 
and  distension  of  the  nasal  veins,  together  with  distension  of  the 
veins  of  the  scalp.  Posteriorly  the  superior  longitudinal  sinus 
ends  at  the  torcular  Herophili, 

The  inferior  longitudinal  sinus  is  quite  small,  and,  like  the 
superior,  lies  between  the  layers  of  the  falx  cerebri,  but  at  its  lower 
edge.  It  runs  backwards  to  the  anterior  edge  of  the  tentorium, 
receiving  branches  from  the  mesial  surface  of  the  hemispheres,  and 


Fig,   29. — Thrombosis  of  left  cavernous  sinus. 

ends  in  the  straight  sinus.  The  straight  sinus  receives  some 
cerebellar  veins  and  the  veins  of  Galen  from  the  velum  inter- 
positum  and  interior  of  the  brain,  and  passes  backwards  either  into 
the  torcular  Herophili  or  into  one  of  the  lateral  sinuses.  When 
the  veins  of  Galen  are  thrombosed  the  cerebral  ventricles  become 
distended  with  fluid. 

The  lateral  sinuses  begin  at  the  internal  occipital  protuberance 
and  arch  outwards,  one  on  each  side,  to  open  through  the  jugular 
foramen  into  the  internal  jugular  vein.  The  sinus  passes  close 
to  the  mastoid  portion  of   the  temporal  bone.      Here  it  receives 


ANATOMY  AND  PHYSIOLOGY  47 

the  superior  petrosal  sinus  ^  and  also  emissary  veins  from  the 
scalp  in  the  mastoid  region.  Just  before  it  empties  into  the 
jugular,  it  receives  the  inferior  petrosal  sinus  and  sometimes  the 
occipital  sinus  from  the  torcular.  Lateral  sinus  thrombosis  is  a 
well-known  and  dangerous  complication  of  suppuration  in  the 
middle  ear.  It  is  recognised  by  distension  of  the  mastoid  veins, 
oedema  of  that  region,  and  hardness  and  tenderness  of  the 
internal  jugular  vein.  Together  with  this  we  may  have  rigidity  of 
the  neck,  tinnitus,  vertigo,  and  even  signs  of  compression  of  the 
vagus,  such  as  dyspnoea,  dysphagia,  bradycardia,  and  palatal 
paresis.  It  is  not  uncommon  to  find  swelling  and  oedema  of  the 
ipso-lateral  optic  disc. 

The  cavernous  sinuses  lie  one  on  each  side  between  the 
sphenoidal  fissure  and  the  apex  of  the  temporal  bone.  Each  sinus 
receives  the  ophthalmic  veins  from  the  orbit  and  communicates 
by  means  of  the  circular  sinus  with  its  fellow  of  the  opposite  side. 
The  sinus  ends  posteriorly  by  opening  into  the  two  petrosal  sinuses. 
Thrombosis  of  the  cavernous  sinus  is  generally  secondary  to  some 
septic  condition  of  the  orbit,  naso-pharynx,  or  sphenoidal  sinus. 
It  is  recognised  by  the  presence  of  chemosis  (oedema  of  the  con- 
junctiva), proptosis  (bulging  forwards  of  the  eyeball),  and  oedema 
of  the  upper  lid  and  root  of  the  nose  (see  Fig.  29).  There  may  be 
paralysis  of  certain  of  the  external  ocular  muscles  from  affection 
of  the  third,  fourth,  or  sixth  nerves  which  lie  in  the  outer  wall 
of  the  cavernous  sinus. 

Nearly  all  the  intra-cranial  venous  blood  leaves  the  skull  by 
the  internal  jugular  veins,  so  that  in  an  infective  thrombosis  of 
any  of  the  cerebral  sinuses  it  may  become  necessary  to  ligature 
the  internal  jugular  vein  to  prevent  a  general  pyaemia. 


CHAPTER   III 

METHOD   OF  CASE-TAKING 

In  no  class  of  maladies  is  a  thorough  examination  of  the  patient 
of  greater  importance  than  in  cases  of  nervous  disease.  One  can- 
not urge  too  strongly  the  value  of  systematic  examination,  though 
it  matters  little  what  particular  scheme  of  case-taking  be  adopted, 
so  long  as  it  is  one  which  ensures  that  the  investigation  is  complete, 
and  that  no  point  of  importance  is  overlooked.  Sometimes,  it  is 
true,  we  may  make  a  diagnosis  at  a  glance,  as  for  example  in 
paralysis  agitans,  or  chorea.  But  more  usually  the  patient  pre- 
sents symptoms  or  signs  which  are  common  to  several  diseases, 
and  we  have  to  decide  from  which  of  these  diseases  he  is  suffering. 
The  chief  causes  of  wrong  diagnosis  are  insufficient  examination, 
inaccurate  observation,  and,  less  commonly,  false  conclusions 
from  correct  and  sufficient  facts.  But  if  we  pursue  a  good  routine 
method  of  examination,  gross  errors  of  diagnosis  can  generally 
be  avoided. 

Examination  of  a  nervous  case  should  not  be  confined  to  the 
nervous  system  alone.  All  the  systems  of  the  body  should  be 
investigated.  An  accomplished  neurologist  must  be  in  the  first 
place  a  sound  physician. 

The  value  of  negative  as  well  as  positive  facts  cannot  be 
over-estimated.  The  neurological  student  should  accustom  him- 
self from  the  outset  not  only  to  chronicle  deviations  from  the 
normal,  but  also,  if  he  finds  that  certain  other  functions  are 
normal,  to  record  the  fact  and  not  to  pass  them  over  without 
reference. 

As  in  any  other  case,  a  careful  history  should  first  be  obtained. 
It  is  comparatively  seldom  that  a  patient,  however  willing  he  may 
be,  provides  us  spontaneously  with  an  accurate  history  of  his 
case.  We  generally  have  to  guide  his  tale  by  suitable  questions, 
and  in  many  cases  we  have  to  supplement  the  patient's  account 


METHOD    OF    CASE-TAKING  49 

by  inquiring  for  corroborative  or  correcting  facts  from  the  patient's 
friends. 

We  first  inquire  as  to  the  mode  of  onset  of  the  patient's 
symptoms,  whether  such  onset  was  sudden  or  gradual,  and,  if 
gradual,  the  exact  order  in  which  the  various  symptoms  appeared. 
In  the  family  history,  inquiry  should  be  made  as  to  the  occur- 
rence of  nervous  or  mental  disease  in  other  members  of  the  family, 
also  as  to  a  family  history  of  gout,  asthma,  tuberculosis,  cancer, 
&c.  In  certain  cases,  consanguinity  of  the  parents  should  be 
inquired  for.  In  the  account  of  the  patient's  previous  health,  it  is 
important  to  inquire  as  to  syphilis,  kidney  disease,  gout,  rheumatic 
fever,  or  any  previous  nervous  disease,  and  a  note  should  be  made 
as  to  the  patient's  occupation  and  habits  of  life,  and  as  to  his 
temperance  in  alcohol,  tobacco,  &c.  When  inquiring  about  venereal 
disease,  if  the  patient  is  a  man,  we  should  put  our  questions  straight- 
forwardly, but  in  female  patients  considerable  deUcacy  is  necessary, 
and  it  is  advisable  simply  to  inquire  for  collateral  symptoms, 
e.g.  rashes,  falKng  out  of  hair,  sore  throat  and,  especially  in  married 
women,  a  succession  of  premature  or  dead  children.  In  any  case 
we  should  never  interrogate  a  male  patient  on  the  subject  of 
venereal  disease  in  the  presence  of  his  wife,   nor  vice  versa. 

Having  thus  noted  the  chief  points  in  the  history  of  the  case, 
we  proceed  to  the  examination  of  the  patient's  'present  state.  The 
following  scheme  will  be  found  useful : — 

Scheme  for  Routine  Examination  of  Nervous  System. 

Higher  Cerehral  and  Mental  Functions. 

Intellectual    functions — Emotional    state — Memory — Hallucinations    or 
delusions — Delirium — Coma — Drowsiness — Insomnia. 

Fits  or  other  Abnormal  Movements. 

Fits  —  Tremors  —  Fibrillary  movements  —  Chorea  —  Athetosis  —  Tic  — 
Myoclonus,  &c.     Description  of  each. 
Speech  and  Articulation. 

Aphasia — Is  patient  right  or  left  handed  ? 
Cranial  Nerves. 

1.  Smell — Anosmia — Parosmia. 

2.  Visual  acuity — Fields  of  vision:  Hemianopia,  &c. — Culour-blindness 

— Ophthalmoscopic  examination — optic  discs,  atrophy,  neuritis — 
retinal  haemorrhages,  choroiditis,' &c. 

D 


50  NERVOUS    DISEASES 

"I  Pupils  :  Size,  shape,  reaction  to  light  (direct  and  consensual),  and 
I        to  accommodation — External  ocular  movements — Ptosis — Move- 
I        ments  of  eyes  in  all  directions — Convergence — Squint  —Diplopia 
■j        — Nj-stagmiis. 
5.  Sensation — Face  :  Conjunctival,  nasal,  and  buccal  mucous  membranes 
—Taste. 
Motor — masseters,  temporals,  pterj'goids,  &c. 

7.  Facial  muscles,  upper  and  lower — Chorda  tympani :  taste  in  anterior 

two-thirds  of  tongue — Nerve  to  stapedius- — hyperacousis. 

8.  Hearing:  Aerial  and  bone  conduction — Examination  of  meatus  and 

tympanic  membrane — Tinnitus — Vertigo. 

9.  Taste  :  Posterior  third  of  tongue — Anaesthesia  of  pharynx — Difficulty 

in  swallowing. 

10.  Palate — Recurrent  hiryngeal  branch — Laryngoscopic   examination — 

Heart,  respiration,  digestion. 

11.  Sterno-mastoid  and  Trapezius. 

12.  Tongue  (motor  only). 

Sensory  Functions. 

Subjective  sensations  :  Pain  : — site,  direction  of  radiation,  character, 
frequency — Headache — Vertigo — Tingling^ — "Pins  and  Needles" 
— Formication,  &c. 

Sensibility  to  touch  —  pain  —  temperature  —  Localisation  of  the  spot 
touched — Yibration-sense  (with  tuning-fork) — Anaesthesia — Par- 
aesthesia — Hypersesthesia — Tenderness  on  pressure  over  nerve- 
trunks,  muscles,  or  skin — Joint-sense — Sense  of  active  muscular 
contraction  with  different  weights — Stereognosis. 

Motor  Functions. 

Paralysis  or  Paresis : — In  head  and  neck,  upper  limbs,  diaphragm,  inter- 
costals,  spinal  and  abdominal  muscles,  lower  limbs. 

Monoplegia — Hemiplegia — Diplegia — Paraplegia — Hemi- para- 
plegia— "  Crossed  paralysis,"  &c. 

Co-ordination : — Unsteadiness  of  upper  or  lower  limbs  on  voluntary  move- 
ment— Gait. 

Muscular  Atrophy  or  Hypertrophy  :  Eigidity— Flaccidity — Hypotonia. 

Reflexes. 

Superficial. — Conjunctival,  palatal,  epigastric,  abdominal,  cremasteric 
plantar  (flexion  or  extension  of  hallux) — bulbo-cavernosus — anal. 

Deep. — Jaw,  wrist,  elbow,  knee,  ankle-jerks.  Ankle-clonus — knee- 
clonus,  &c. 

Organic. — Micturition — Pvetention- — Eetentiun  with  overflow  incontinence 
—  Intermittent  incontinence  —  Constant  paralytic  dribbling— 
Defaecation — Control  of  sphincters — Priapism. 

TropMc  Functions. 

Muscles. — Electrical  reactions — Faradic — Galvanic. 

Skin. — Bulhe — Herpes — Bed-sores — Perforating  ulcers— Glossy  skin,  &c. 
Joints  and  Bones. — Charcot's  arthropathy — Spontaneous  fractures — Pes 
cavus,  &c. 


METHOD    OF    CASE-TAKING  51 

Examination  of  Skull  and  Vertebral  Column. 

Abnormal  projections  or  depressions — Tenderness,  &c.,  on  peicussion. 

Cerebro-spinal  Fluid, 

Naked-eye  characters  of  fluid — Microscopic  examination — Bacteriological 
characters — Chemical  reactions,  &c. 

Sympathetic  Nervous  System. 

Cervical  sympathetic — Dilatation  of  pupil  to  shade  and  cocaine — Cilio- 
spinal  reflex  —  Proptosis  —  Exophthalmos  —  Enoplithalmos — Re- 
traction of  upper  lid — Pseudo-ptosis — Flushing  or  sweating  of 
face,  neck,  upper  extremity. 

Angio-neuroses — Raynaud's  disease — Erythromelalgia — Angio-neurotic 
cedema — Localised  hyperidrosis  or  anidrosis — Intermittent  claudi- 
cation, &c. 

Several  points  should  be  noticed  in  the  foregoing  scheme.  We 
begin  with  the  higher  cerebral  and  mental  functions,  for  this 
reason,  that  if  a  patient  be  mentally  obtuse,  or  worse,  if  he 
be  delirious,  then  any  statement  he  may  make  is  open  to 
doubt,  and  for  our  diagnosis  we  must  rely  mainly,  and  in  cases 
of  coma  entirely,  upon  physical  signs  and  upon  the  history 
supplied  by  the  patient's  friends. 

The  patient's  emotional  state  is  sometimes  of  diagnostic  signifi- 
cance. Not  only  are  many  hysterical  patients  unduly  emotional, 
but  a  similar  condition  is  observed  in  certain  cases  of  disseminated 
sclerosis,  where  there  is  a  tendency  to  smile  and  giggle  upon  shght 
provocation,  whilst,  on  the  other  hand,  cases  of  aphasia  and  of 
advanced  bulbar  palsy  are  often  lachrymose. 

The  statements  of  a  patient  who  is  addicted  to  alcohohc  in- 
temperance or  to  chronic  poisoning  with  opium,  cocaine  or  other 
drug,  must  also  be  received  with  considerable  scepticism.  There 
is  a  special  variety  of  loss  of  memory,  called  Korsakoiv's  'psychosis, 
which  occurs  chiefly  in  chronic  alcohoKcs,  where  the  patient, 
who  is  usually  a  woman  and  the  subject  of  peripheral  neuritis 
(most  commonly  alcoholic,  but  sometimes  due  to  other  causes, 
such  as  arsenic,  septic  absorption,  &c.),  has  a  faulty  conception 
of  time  and  place  and  a  specially  deficient  memory  for  recent 
events.  Moreover  she  frequently  has  what  are  euphemistically 
called  "  pseudo-memories,"  so  that  "  the  truth  is  not  in  her." 
This  is  one  of  the  toxic  varieties  of  insanity,  and  is  commoner  in 
women  than  in  men.     Male  alcohohcs    seldom    show  Korsakow's 


52  NEEVOUS    DISEASES 

psycliosis,  but  tend  rather  to  suffer  from  the  more  violent  and 
dramatic  "delirium  tremens,"  with  the  tremors,  acute  distress,  and 
hallucinations  of  rats,  beetles,  devils,  &c.  (zoopsia),  so  familiar 
to  the  lay  writer. 

Passing  from  the  patient's  mental  condition,  we  should  carefully 
observe  and  describe  any  fits,  tremors,  or  other  spontaneous 
abnormal  movements  that  may  be  present.  Disorders  of  speech 
and  articulation  should  next  be  studied,  and  the  cranial  nerves 
examined  in  due  order. 

It  will  be  observed  that,  in  our  scheme  of  case-taking,  sensory 
functions  are  investigated  before  motor.  As  a  matter  of  experi- 
ence, this  order  of  examination  is  found  to  be  of  considerable 
practical  advantage.  The  discovery  of  an  area  of  anaesthesia 
often  puts  us  rapidly  on  the  track  of  a  correct  diagnosis  and 
enables  us  to  select  with  greater  ease  the  saUent  points  in  the 
motor  and  other  phenomena. 

Certain  accessory  methods  of  examination,  such  as  the  testing 
of  electrical  reactions  and  lumbar  puncture,  are  required  only 
in  special  circumstances,  where  they  may  throw  a  flood  of  hght  on 
an  otherwise  obscure  case.  Inspection,  palpation,  and  percussion 
of  the  skull  are  of  considerable  value  in  some  cases  of  tumour  of 
the  brain,  especially  in  cases  of  cerebellar  growths.  Sometimes  it 
is  advisable  to  have  the  scalp  shaved,  in  order  to  detect  abnor- 
malities in  the  shape  of  the  cranium. 

Having  collected  our  facts,  comprising  the  history  and  the 
present  state  of  the  patient,  we  are  now  in  a  position  to  make  our 
diagnosis.  And  in  the  process  of  diagnosis  we  have,  first  of  all, 
to  ask  ourselves — Is  the  disease  an  organic  one,  due  to  a  gross 
irritative  or  destructive  lesion  in  the  nervous  system,  for 
example  cerebral  haemorrhage,  alcoholic  neuritis  or  tubercidous 
meningitis  ?  Or  is  it  one  of  the  so-caUed  "  functional "  diseases, 
that  is  to  say,  without  known  morbid  anatomy,  for  example 
hysteria,  migraine,  neurasthenia  ?  ^ 

If  the  evidence  points  to  an  organic  lesion,  we  have  then  to 

1  The  boundary-line  between  functional  and  organic  diseases  is  not  so 
definite   as  might   at  first  sight  be   supposed.     At  the  present    day,   many 


METHOD    OF    CASE-TAKING  53 

ask  ourselves  two  further  questions :  (1)  Where  is  the  lesion  ? 
(2)  What  is  its  pathological  nature  ?  The  answer  to  the  first 
question,  which  constitutes  the  anatomical  diagnosis,  is  derived 
mainly  from  a  study  of  the  distribution  and  grouping  of  the  signs 
and  symptoms.  The  answer  to  the  second,  constituting  the  'patho- 
logical diagnosis,  is  attained  mainly  by  a  study  of  the  history  of 
the  mode  of  onset. 

In  making  an  anatomical  diagnosis  we  should  always  endeavour 
to  think  of  a  single  lesion  which  will  account  for  all  the  symptoms. 
Thus,  for  example,  if  a  patient  comes  to  us  with  hemiplegia  of  the 
left  arm  and  leg,  of  the  "  upper  motor  neurone  "  type  (see  p.  28), 
and  at  the  same  time  a  right- sided  facial  palsy  of  the  "  lower 
motor  neurone "  type,  instead  of  diagnosing  two  lesions,  one 
in  the  right  side  of  the  brain  causing  left  hemiplegia  and  another 
in  the  right  facial  nerve  causing  right  facial  palsy,  we  prefer 
to  diagnose  a  single  lesion  in  the  right  side  of  the  pons,  impli- 
cating simultaneously  the  right  facial  nerve  and  the  pyramidal 
tract  (see  Fig.  6). 

As  an  example  of  pathological  diagnosis,  suppose  we  have  a 
patient  with  spastic  paraplegia  of  both  lower  limbs  and  anaesthesia 
up  to  the  level  of  the  umbilicus,  the  anatomical  position  of  the 
lesion  is  comparatively  easy  to  fix,  namely  in  the  lower  thoracic 
region  of  the  cord,  implicating  both  sensory  and  motor  tracts.  If  the 
symptoms  appeared  suddenly,  we  think  of  a  vascular  lesion  such 


diseases  are  classified  as  functional,  for  no  better  reason  than  that  in  them 
no  constant  anatomical  changes  have  yet  been  recognised.  In  such  diseases 
as  epilepsy,  paralysis  agitans,  exophthalmic  goitre,  and  Raynaud's  disease, 
there  can  be  little  doubt  that  profound  molecular  changes  exist — in  the 
two  former  instances  in  the  central  nervous  system,  in  the  two  latter 
in  the  sympathetic  system — but  these  changes  have  not  yet  been  recog- 
nised. Other  diseases  again,  due  to  poisoning  by  microbes  or  their  toxins, 
or  by  other  poisons — e.g.  chorea,  hydrophobia,  tetanus,  certain  varieties 
of  epileptiform  fits,  &c. — are  undoubtedly  the  resvdt  of  pathological  changes 
affecting  various  groups  of  nerve  elements.  And  yet,  because  at  present  these 
changes  are  not  visible  histologically,  they  have  been  classed  as  "  functional." 
Even  hysteria  itself,  the  prototype  of  functional  diseases,  has  some  profound 
underlying  bio-chemical  change.  The  term  "  functional,"  then,  is  a  confession 
of  our  etiological  ignorance,  and  is  by  no  means  synonymous  with  "  curable," 
as  the  steady  and  progressive  advance  of  such  a  disease  as  paralysis 
agitans  readily  shows. 


54  NERVOUS    DISEASES 

as  haemorrhage  or  thrombosis ;  if  they  developed  within  a  day  or 
two,  some  inflammatory  condition  such  as  myehtis  is  probable  ; 
whilst  if  they  only  appeared  very  slowly,  taking  many  months 
to  reach  their  present  intensity,  we  have  to  think  of  a  slowly  pro- 
gressive lesion,  such  as  a  tumour. 

We  must  never  diagnose  hysteria  or  neurasthenia  until  we 
have  excluded  gross  organic  disease.  And,  finally,  we  should 
remember  that  the  presence  of  certain  hysterical  or  neurasthenic 
symptoms  does  not  exclude  a  co-existent  organic  lesion,  nor  vice 
versd.  Functional  and  organic  disease  may  be  combined  in  the 
same  patient,  and  this  combination  increases  the  difficulty  of 
diagnosis. 


CHAPTER   IV 

COMA 

We  are  not  infrequently  called  to  see  a  patient  who  is  found  to  be 
unconscious.  In  such  cases  it  is  of  great  importance  to  make  a 
correct  diagnosis  as  to  the  probable  cause.  There  are  different 
degrees  of  unconsciousness.  For  example,  there  are  conditions 
in  which  the  patient  can  be  roused  from  his  unconsciousness 
by  shaking,  shouting,  or  other  stimuli,  as  in  the  case  of  ordinary 
sleep.  When  this  degree  of  unconsciousness  occurs  in  pathological 
conditions,  as  in  a  patient  stupefied  by  various  poisons  (whether 
produced  within  the  body  or  introduced  from  without),  or  from 
mechanical  compression  of  the  brain,  for  example  by  haemorrhage, 
we  call  the  condition  stupor. 

Cerebral  Concussion,  resulting  from  head-injury,  is  a  condition 
in  which  the  patient  is  pale  and  collapsed,  with  a  low  blood-pressure. 
He  may  be  stuporose  or  even  comatose.  In  a  slight  case  there  is 
merely  temporary  unconsciousness  or  giddiness,  with  pallor  and 
a  little  mental  confusion,  often  followed  by  headache.  In  more 
severe  cases  there  is  an  initial  stage  of  collapse  with  unconsciousness 
lasting  for  hours  or  even  for  days.  But  in  most  cases  the  patient 
can  be  roused  by  strong  stimuli.  His  face  is  pale,  his  breathing 
is  slow,  shallow,  and  irregular  ;  his  pulse  is  weak  and  his  temperature 
subnormal.  He  hes  with  flaccid  limbs,  hke  a  drunken  man. 
Trendelenburg  has  aptly  named  this  condition  "  traumatic 
narcosis."  Then  comes  the  stage  of  reaction,  often  ushered  in  by 
vomiting,  sometimes  even  by  an  epileptiform  convulsion.  Con- 
sciousness begins  to  return  ;  the  temperature  rises  and  may  mount 
to  100°  F.  or  higher,  the  pulse  is  now  full  and  bounding,  and  the 
respirations  become  deeper.  There  is  usually  headache.  Such  a 
patient  generally  has  a  "  retrograde  amnesia,"  i.e.  he  has  no 
recollection  of  the  incidents  which  occurred  within  the  last  few 
hours  immediately  prior  to  his  accident.     As  a  rule,  although  the 


56  NEKVOUS   DISEASES 

memory  of  these  incidents  returns  later,  the  remembrance  of  the 
accident  itself  is  permanently  lost. 

Coma  is  that  degree  of  unconsciousness  which  is  so  deep  that 
we  are  unable,  by  any  ordinary  stimulus,  to  rouse  the  patient. 
A  deeply  comatose  patient  does  not  swallow  fluids  placed  in  his 
mouth,  his  conjunctival  reflexes  are  absent  and  his  pupils  in- 
sensitive to  Ught,  as  in  deep  chloroform  anaesthesia. 

How  are  we  to  proceed  when  called  to  see  a  patient  whom 
we  find  comatose  ?  Firstly,  we  inquire  into  the  history,  as  to  the 
patient's  previous  health,  whether  the  coma  was  sudden  or  gradual 
in  onset  and  whether  it  was  preceded  by  other  symptoms,  such  as 
convulsions  or  headache.  We  then  examine  the  patient,  feel  the 
head  for  signs  of  injury,  smell  the  breath,  examine  the  pupils, 
noting  their  size,  equality  or  inequality,  and  their  reaction  to 
light ;  we  listen  to  the  heart  and  note  the  character  and  frequency 
of  the  pulse  and  respirations.  We  note  the  radial  blood-pressure 
and,  if  possible,  measure  it  by  means  of  a  Riva-Rocci  sphygmo- 
manometer. We  observe  whether  the  face  is  symmetrical  or 
not,  and  whether  there  is  conjugate  deviation  of  the  head  and 
eyes  in  any  direction.  The  optic  discs  in  all  cases  should 
be  examined.  We  hft  the  limbs  in  turn  and  let  them  fall, 
observing  whether  there  is  any  difference  between  the  flaccidity 
of  the  two  sides.  We  also  test  the  knee-jerks  and  examine  the 
abdominal  and  plantar  reflexes  on  both  sides.  Then  we  pass  a 
catheter,  draw  off  the  urine,  note  its  specific  gravity  and  test 
it  for  albumen  and  for  sugar.  Finally  we  note  the  temperature 
in  both  axillse,  and  in  certain  cases  we  perform  lumbar  puncture 
and  examine  the  cerebro- spinal  fluid. 

The  first  question  is  whether  the  coma  is  due  to  a  general 
toxaemia,  such  as  poisoning  by  alcohol  or  opium,  uraemia,  dia- 
betes, &c.,  or  whether  it  is  the  result  of  some  gross  intra-cranial 
lesion,  such  as  haemorrhage,  meningitis,  abscess,  tumour,  &c. 

As  a  general  maxim  we  may  state  that,  if  coma  be  toxsemic  in 
origin,  practically  all  the  signs  and  symptoms  will  be  bilaterally 
symmetrical.  On  the  contrary,  most  cases  of  gross  intra-cranial 
disease  being  unilateral,  or  at  least  asymmetrical,  there  will  there- 


COMA  57 

fore  be  a  corresponding  preponderance  of  symptoms  on  one  side 
of  tlie  body,  so  that,  in  addition  to  coma,  we  have  a  number  of 
unilateral  signs.    Let  us  consider  these  unilateral  cases  first. 

The  commonest  case  is  that  of  spontaneous  cerebral  hsemorrhage. 
Here  the  onset  of  unconsciousness  is  generally  sudden ;  the 
patient's  face  is  flushed  or  cyanosed,  his  skin  sweats  profusely, 
he  breathes  stertorously,  his  blood-pressure  is  high,  and  his  pulse 
is  slow,  full  and  bounding.  All  his  limbs  are  flaccid,  but  on 
comparing  the  two  sides,  we  find  that  the  flaccidity  is  more 
absolute  on  the  hemiplegic  side.  For  example,  the  elbow  of  the 
affected  side  can  be  passively  flexed  to  a  greater  degree  than 
that  of  the  healthy  side.  The  arm  and  leg  on  the  paralysed 
side  also  fall  more  "  dead "  than  do  those  of  the  sound  side 
when  hfted  up  in  turn  and  allowed  to  drop.  The  paralysed 
leg  Kes  extended,  whereas  the  healthy  one  tends  to  be  semi- 
flexed. The  head  and  eyes  are  often  turned  to  one  side, 
generally  away  from  the  paralysed  limbs,  unless  the  hsemorrhage 
be  cortical  or  intra-ventricular,  in  which  cases  the  deviation 
may  be  toward  the  paralysed  limbs,  and  is  associated  with 
other  irritative  phenomena,  e.g.  spasticity  instead  of  flac- 
cidity. The  face  is  asynimetrical,  especially  its  lower  part,  the 
paralysed  cheek  flaps  loosely  during  respiration  and  the  mouth 
is  distorted  like  a  mark  of  exclamation  laid  on  its  side  (!— )?  ^^  i^ 
the  patient  were  "  pufflng  his  pipe  "  at  the  paralysed  angle  of  the 
mouth.  The  pupils  are  generally  dilated  and  sometimes  unequal, 
the  larger  pupil  being  on  the  side  of  the  brain  lesion.  In  pontine 
haemorrhage,  however,  the  pupils  are  often  contracted  to  pin- 
points. At  the  onset  of  an  ordinary  apoplexy,  whilst  we  get  little 
help  from  the  deep  reflexes,  which  may  or  may  not  be  diminished 
or  lost  on  the  affected  side,  there  is,  from  the  very  outset, 
an  extensor  plantar  reflex  in  the  toes  of  the  hemiplegic  foot,, 
and  all  the  other  superficial  reflexes  on  that  side  are  diminished 
or  absent.  The  skin  of  the  abdomen  can  be  pinched  or  pricked 
on  the  paralysed  side  without  ehciting  an  abdominal  reflex — 
(Rosenbach's  sign).  The  corneal  reflex  is  abohshed  on  the  hemi- 
plegic  side   instead  of   on  both  sides   as   in   toxic  coma.      The 


58  NERVOUS    DISEASES 

temperature  on  the  paralysed  side  is  usually  higher  than  on  the 
other,  although  the  general  temperature  of  the  whole  body  falls 
at  first.  If  the  coma  has  lasted  several  hours,  the  bladder  becomes 
distended  and  may  develop  an  overflow  incontinence.  Afterwards, 
the  temperature  rises  above  normal,  and  in  bad  cases  may  go  on 
to  hyper-pyrexia. 

Most  cases  of  spontaneous  cerebral  haemorrhage  occur  in  patients 
past  middle-age,  in  whom  the  arteries  are  no  longer  elastic  and 
healthy,  and  there  is  often  a  history  of  kidney  disease,  with  its 
resultant  cardiac  hypertrophy  and  high-tension  pulse,  conditions 
particularly  liable  to  result  in  the  bursting  of  a  cerebral  artery. 
The  actual  attack  of  hsemorrhage  not  uncommonly  occurs  during 
some  slight  physical  exertion  or  mental  excitement,  as  in  public 
speakers,  such  as  clergymen,  politicians,  or  after-dinner  orators, 
or  in  old  men  with  brittle  arteries,  during  straining  at  stool.  In 
most  cases  of  intra-dural  cerebral  haemorrhage  from  whatever 
cause,  the  cerebro-spinal  fluid  is  tinged  with  blood  in  greater  or 
smaller  amount  (see  later,  p.  407). 

But  cerebral  haemorrhage  may  also,  in  rare  cases,  occur  in  young 
people  having  healthy  vessels,  as,  for  example,  in  a  child  during 
violent  convulsions  or  during  a  paroxysm  of  whooping-cough,  where 
the  haemorrhage  is  commonly  venous  and  due  to  passive  congestion 
with  rupture  of  the  cortical  veins,  or  it  may  occur  in  any  of  the  so- 
called  "  bleeding  diseases  " — purpura,  haemophilia,  leukaemia,  &c. 

Cerebral  haemorrhage  often  occurs  in  cases  of  general  paralysis 
of  the  insane,  and  in  fact  may  be  the  first  symptom  calling 
attention  to  the  disease.  The  symptoms  are  those  already 
described,  but  there  is  usually  a  history  of  previous  mental 
failure,  grandiose  ideas,  loss  of  memory,  attacks  of  emotional 
excitement,  and  shght  indistinctness  of  articulation.  In  the 
absence  of  such  history,  we  may  be  unable  at  the  time  to  diagnose 
anything  more  than  the  fact  of  a.  cerebral  haemorrhage.  But 
afterwards,  when  the  patient  recovers  from  his  apoplexy — and  the 
general  paralytic  recovers  much  more  rapidly  than  the  non-insane 
patient — ^we  can  generally  recognise  the  characteristic  evidences 
of  the  disease,  both  psychical  and  physical. 


COMA  59 

Coma  may  also  be  due  to  traumatic  cerebral  "compression," 
where  there  is  a  haemorrhage  on  the  surface  of  the  brain,  either 
intra-  or  extra-dural.  The  signs  are  practically  the  same  as  in 
spontaneous  apoplexy  but  the  onset  is  different,  for  there  is  a 
history  of  a  head  injury.  The  symptoms  develop  gradually, 
especially  if  the  hsemorrhage  be  extra-dural,  beginning  with  local 
paralysis  and  perhaps  localised  convulsions.  The  paralysis  gradually 
increases,  the  patient  becomes  drowsy,  stupid,  and  finally  comatose, 
the  blood-pressure  meanwhile  rising  to  an  excessive  degree.  There 
may  be,  before  the  onset  of  coma,  a  "  lucid  interval "  of  several 
hours  or  even  a  whole  day,  during  which  the  patient,  who  was 
perhaps  only  stunned  by  the  original  blow,  recovers  consciousness 
and  is  apparently  normal.  A  lucid  interval,  when  followed  by 
the  above  symptoms,  generally  indicates  that  the  haemorrhage  is 
extra-dural.  In  intra-cranial  haemorrhage  oedema  of  the  retina 
often  supervenes  within  a  few  hours. ^  This  oedema  is  more  intense 
in  the  eye  on  the  same  side  as  the  focal  compression,  and  the  fact 
may  be  of  diagnostic  value  in  obscure  cases  of  coma  following  head- 
injuries.  This  retinal  oedema  rapidly  subsides  if  the  intra-cranial 
tension  be  relieved  by  operation.  It  is  uncommon  for  symptoms 
of  compression  to  come  on  immediately  after  the  head  injury, 
and  when  they  do  so,  they  suggest  a  depressed  fracture  pressing 
directly  on  the  brain.  This  can  generally  be  detected  by  examina- 
tion of  the  cranium. 

Pontine  Hsemorrhage  is  generally  near  the  middle  hne,  and 
therefore  tends  to  produce  bilateral  symptoms.  Pontine  cases 
generally  (but  not  always)  have  strongly  contracted  pupils  owing 
to  irritation  of  the  third  nerve  nuclei.  There  is  often  hyper- 
pyrexia and  most  cases  are  fatal. 

Thrombosis  of  the  Cerebral  Sinuses  is  a  rarer  cause  of  coma. 
Here  the  diagnosis  rests  chiefly  on  the  history.  Cases  secondary 
to  suppurative  conditions  of  the  middle  ear  or  frontal  sinuses  will 
have  a  corresponding  history  and  the  other  signs  of  intra-cranial 
venous  obstruction.  Primary  thrombosis  of  a  sinus,  occurring 
without  infection,  as  in  marasmus,  profound  anaemia,  &c.,  is  ex- 

^  Gushing,  New  York  Medical  Journal,  January  19,  1907. 


60  NERVOUS    DISEASES 

cessively  difficult  to  recognise.  Thrombosis  of  cerebral  arteries, 
producing  cerebral  softening,  often  causes  hemiplegia,  but  its  onset 
is  slower  than  is  that  of  haemorrhage ;  it  more  often  comes  on 
during  ordinary  sleep  and  is  rarely  associated  with  coma.  In 
young  patients  it  is  generally  syphiUtic  in  origin. 

Amongst  the  other  gross  intra-cranial  diseases  producing  coma, 
there  is  cerebral  meningitis.  Here  again  our  diagnosis  depends 
on  the  history.  Most  frequently  the  patient  is  a  child.  Instead  of 
a  history  of  sudden  coma  or  of  head  injury  we  learn  that  there  have 
been,  for  some  days,  headache,  vomiting,  photophobia  and  head- 
retraction,  and  often  the  characteristic  "  hydrocephalic  cry."     The 


Fig.  30. — Case  of  posterior  basic  meningitis,  showing  head-retraction 
and  posture  of  limbs. 

child  gradually  becomes  drowsy,  apathetic,  and  finally  comatose. 
Rigidity  of  the  neck  muscles  and  head-retraction  persist  during 
the  coma  (Fig.  30).  Kernig's  sign  and  Brudzinski's  "  neck  "  and 
"  leg  "  signs  are  often  of  value.  Kernig's  sign  consists  in  a  reflex 
contraction  of  the  hamstring  muscles  and  a  wince  of  pain  when  an 
attempt  is  made  to  put  the  sacral  nerve-roots  on  the  stretch  by 
flexing  the  hip  to  a  right  angle  and  at  the  same  time  extending 
the  knee.  Brudzinskis  necJc-sign,  which  is  even  more  frequently 
present  than  Kernig's  sign,  is  ehcited  by  first  flexing  the  arms  and 
legs  on  the  trunk  to  their  full  extent  and  then  passively  flexing  the 
head  on  the  chest.  The  patient  at  once  cries  out,  Brudzinski's 
leg-sign  is  elicited  by  passively  flexing  one  lower  limb  on  the  abdomen 
to  its  full  extent,  when  the  other  leg  is  at  once  drawn  up  by  the 


COMA  61 

patient  to  a  similar  position.  If  the  meningitis  be  chiefly  on  the 
convexity  of  the  brain,  there  are  commonly  convulsions  precedmg 
or  accompanying  the  coma.  On  the  other  hand,  if  the  meningitis 
be  mamly  basal,  there  are  cranial  nerve  paralyses,  especially  of  the 
ocular  muscles.  Examination  of  the  cerebro-spinal  fluid  obtained 
by  lumbar  puncture  gives  conclusive  evidence  in  cases  of  suspected 
meningitis.  Optic  neuritis,  if  present,  will  indicate  that  the  coma 
is  not  due  to  mere  haemorrhage,  but  that  there  is  increased  intra- 
cranial pressure,  either  due  to  meningitis,  cerebral  abscess,  or 
possibly,  if  the  history  be  a  matter  of  weeks  or  months,  to  intra- 
cranial growths,  syphihtic,  tuberculous,  or  neoplastic. 

Let  us  now  pass  to  the  other  class  of  cases  of  coma,  due  not 
to  a  gross  intra-cranial  lesion,  but  to  some  general  toxic  condition 
of  the  higher  cerebral  centres.  In  this  group  the  important 
point  to  notice  is  the  absence  of  unilateral  signs. 

In  the  coma  of  opium  poisoning  there  may  be  a  history  of 
laudanum  swallowed  or  morphine  injected  hypodermicaUy.  An 
empty  laudanum-bottle  or  a  hypodermic-syringe  may  be  found 
by  the  patient's  side  when  he  is  discovered.  If  laudanum  has 
been  taken  by  the  mouth,  its  odour  may  be  detected  in  the 
breath.  A  chemical  analysis  of  the  stomach-contents  obtained 
by  the  stomach-tube,  will  also  help  in  the  diagnosis.  In  the 
comatose  patient  we  notice  the  excessive  slowness  of  respiration, 
the  slow  and  feeble  pulse,  the  cold  clammy  skin,  and,  most  striking 
of  all,  the  pupils  contracted  to  pin-points.  These  symptoms  might 
be  confused  with  those  of  pontine  haemorrhage.  But  there  is  not 
the  pyrexia  of  a  pontine  apoplexy,  and  the  coma  of  opium  is  not 
so  deep  as  that  of  haemorrhage.  Moreover,  in  opium-poisoning 
the  plantar  reflexes  are  of  the  normal  flexor  type. 

The  coma  of  acute  alcoholic  poisoning  is  not  so  deep  as  that 
of  apoplexy,  for  the  patient  can  generally  be  roused,  temporarily 
at  least,  by  energetic  stimulation.  The  typical  stertor  of  apoplexy 
is  not  present,  the  pupils  are  dilated  and  react  to  light,  and  the 
corneal  reflexes  are  preserved.  The  temperature  is  subnormal, 
the  breath  and  stomach- contents  smefl  of  alcohol,  and  if  we  mix 
a  specimen  of  the  urine  with  potassium-bichromate  solution  and 


62  NERVOUS    DISEASES 

then  allow  strong  sulphuric  acid  to  flow  to  the  bottom  of  the  test- 
tube,  a  green  colour  appears  if  alcohol  be  present  in  the  urine. 

We  must  be  careful,  however,  not  to  diagnose  alcoholic  poison- 
ing simply  because  the  patient's  breath  smells  of  alcohol.  In  the 
first  place,  a  patient  with  cerebral  haemorrhage  may  have  had 
alcohol  given  him,  just  at  the  onset  of  his  symptoms.  Or  secondly, 
a  patient  who  has  been  drinking  alcohol  may  have  an  attack  of 
apoplexy,  or  he  may  fall  and  sustain  a  head  injury  causing  com- 
pression. Therefore  every  patient  with  apparent  alcohohc  coma 
should  be  carefully  watched  for  about  twenty-four  hours,  in  case 
unilateral  paralysis,  an  extensor  plantar  reflex,  or  inequahty  of  the 
pupils  should  supervene. 

Post-epileptic  Coma  may  be  mistaken  for  apoplexy,  if  we  do 
not  happen  to  know  that  the  patient  is  epileptic.  But  generally 
we  have  the  history  of  preceding  fits,  and  in  a  chronic  epileptic 
there  may  be  old  scars  about  the  scalp,  tongue,  or  face,  the  result  of 
injuries  during  previous  fits.  There  is  no  preponderance  of  uni- 
lateral symptoms  after  a  general  epileptic  fit,  nor  is  there  inequality 
of  the  pupils.  The  tongue  may  have  been  bitten  during  the  fit  and 
may  be  still  bleeding  during  the  stage  of  coma.  Within  an  hour  or 
less,  the  epileptic  recovers  consciousness  without  paralytic  sequelae. 
If,  however,  some  transient  locaHsed  motor  weakness  follows,  this 
points  rather  to  a  Jacksonian  fit  due  to  a  focal  lesion. 

In  the  Stokes-Adams  syndrome  we  have  profound  coma  and 
stertorous  breathing,  with  or  without  epileptiform  convulsions. 
The  condition  is  readily  diagnosed  by  recognition  of  the  extremely 
slow  pulse-rate.  Acceleration  of  the  pulse  precedes  recovery  from 
the  coma. 

Ursemic  Coma  is  not  uncommon,  occurring  as  it  does  in 
patients  who  are  the  subjects  of  nephritis,  acute  or  chronic. 
The  coma  is  usually  preceded  by  ursemic  headaches,  vomiting, 
and  convulsions,  local  or  general.  A  history  of  previous  renal 
disease  is  here  of  great  value.  And  there  may  be  obvious 
signs  of  renal  dropsy  about  the  face  and  legs.  Eespiration  is 
frequently  of  the  Cheyne-Stokes  type.  The  breath  often  has  a 
urinous  cdour,  and  a  catheter  specimen  of  urine  will  show  albumen 


COMA  63 

together  with  various  kinds  of  casts,  and,  in  acute  nephritis, 
blood.  But  we  must  not  forget  that  a  patient  with  chronic 
renal  disease,  a  high-tension  pulse  and  a  hypertrophied  heart,  is 
just  the  one  in  whom  cerebral  haemorrhage  may  fairly  be 
expected.  Therefore  in  a  case  of  coma,  mere  albuminuria  should 
not  lead  us  to  diagnose  uraemic  coma.  We  must  always  be  on 
the  look-out  for  symptoms  of  unilateral  paralysis. 

Diabetic  Coma  is  easy  to  recognise,  if  we  know  that  the  patient 
has  been  suf!ering  from  diabetes.  Even  if  there  be  no  history 
of  diabetes,  examination  of  the  urine  shows  the  characteristic 
high  specific  gravity,  together  with  the  presence  of  sugar  in  large 
amount  as  shown  by  the  ordinary  tests.  The  addition  of  a 
few  drops  of  liq.  ferri  perchloridi  to  the  urine  produces  a  deep 
brownish-red  colour,  due  to  di-acetic  acid.  The  "  acetone  "  smell 
of  the  breath  is  unmistakable  and  occurs  only  in  diabetes,  in  the 
rare  condition  of  "  delayed  poisoning  by  anaesthetics,"  ^  and  in  the 
"  cyclical  or  periodic  vomiting  "  with  acetonuria  seen  in  children,^ 
both  of  which  latter  conditions  are  associated  with  acute  fatty 
changes  in  the  liver.  Further,  diabetic  coma  is  not  sudden  in  onset, 
but  is  commonly  preceded  by  headache,  irritability  and  uncon- 
trollable drowsiness,  merging  into  profound  coma  with  remarkably 
deep  noisy  breathing.  The  pulse  is  usually  small  and  rapid,  unlike 
the  full,  slow  pulse  of  cerebral  haemorrhage.  Rise  of  temperature, 
which  is  so  common  in  cerebral  haemorrhage,  does  not  occur  in  dia- 
betic coma. 

Sunstroke  sometimes  causes  coma.  Here,  of  course,  it  is 
essential  that  there  should  he  a  history  of  exposure  to  a  hot 
sun,  of  a  previously  healthy  patient.  Alcoholic  patients  are  more 
liable  to  sunstroke  than  teetotalers.  A  patient  who  is  comatose 
from  sunstroke  often  has  extraordinary  hyperpyrexia — 108°  F, 
and  upwards.  General  convulsions  may  occur.  The  cerebro- 
spinal fluid  in  such  cases  often  shows  evidences  of  acute  meningeal 
reaction,  in  the  form  of  a  polynuclear  leucocytosis,  passing  on 
subsequently  to  lymphocytosis. 

1  Guthrie,  Clinical  Journal,  June  12,  1907. 

^  Langmead,  British  Medical  Journal,  1905,  p.  3£0. 


64  NEEVOUS    DISEASES 

In  malarial  climates  we  must  also  be  prepared  to  meet  with  a 
comatose  variety  of  pernicious  malaria,  where  the  parasites  produce 
thrombosis  of  the  smaller  cortical  vessels.  A  malarious  patient  may 
rapidly  become  comatose  and  die  within  a  few  hours,  as  happened 
to  a  friend  of  my  own.  In  such  cases  the  malarious  history  and 
the  examination  of  the  blood  for  the  plasmodium  will  settle  the 
diagnosis.  A  patient  dying  from  cancer  may  become  comatose 
shortly  before  death — the  so-caUed  coma  carcinomatosum. 

We  need  not  do  more  than  mention  the  terminal  coma  of  such 
diseases  as  acute  yellow  atrophy,  or  the  "  coma- vigil "  of  typhus 
and  of  severe  enteric  fever. 

Hysterical  Trance,  by  a  careless  observer,  might  be  mistaken 
for  true  coma.  The  hysterical  patient,  however,  has  neither  stertor 
nor  cyanosis,  the  breathing  and  heart's  action  are  regular, 
though  perhaps  very  faint,  the  pupils  react  to  light  and  the  patient 
generally  resists  forcible  opening  of  the  eyes.  Thus  a  young  man 
of  twenty-two  who  had  sudden  attacks  of  apparent  sleep  (narco- 
lepsy) coming  on  in  the  middle  of  meals  or  when  playing  cards, 
refused  to  be  roused  by  ordinary  stimuli  in  the  form  of  shaking  or 
shouting,  but  yielded  at  last  to  forcible  digging  in  the  ribs.  He 
passed  through  a  stage  of  "  grande  hysteric  "  before  waking  up, 
and  for  some  time  afterwards  had  hysterical  blindness  and  other 
hysterical  stigmata. 

The  hypnotic  trance  may  be  regarded  as  an  artificially-induced 
form  of  hysteria,  the  result  of  suggestion  in  a  highly  sensitive 
subject. 


CHAPTER   V 

FITS   AND   OTHER   CONVULSIVE   PHENOMENA 

We  are  often  consulted  about  patients  who  are  said  to  have  "  fits," 

but  we  are  seldom  fortunate  enough  to  witness  an  attack.     If 

we   do,   the  diagnosis  presents    little    difficulty.     More   often,   in 

making   the   diagnosis    as    to   the  nature   of   a  fit,    we   have  to 

depend  upon  the  description  given  by  the  patient's  friends. 

The  following  is  a  Kst  of  the  chief  clinical  conditions  in  which 

convulsive  phenomena  occur  : — 

r Hysteria  major. 

I  Catalepsy. 

j  Hysteria  minor. 

I  Post-epileptic  hysterical  attacks. 


CEREBRAL  FITS  - 


Hysterical 


1^  Epileptiform 


Epilepsy  major  {grand  mal). 
Epilepsy  minor  (j^etit  mal). 
Post-epileptic  automatism — "  masked 

epilepsy." 
Toxic     conditions  : — Asphyxia,    urse- 

mia,  puerperal  eclampsia,  alcohol, 

absinthe,  lead,  &c. 
General  paralysis  of  the  insane. 
Psychasthenia. 
Organic     brain     lesions — Jacksonian 

fits,  &c. 

fToxic. 


Infantile  Convulsions 
Stokes-Adams'  disease. 


(^Organic. 


CEREBELLAR  FITS. 


In  making  inquiries  about  convulsive  phenomena,  whatever 
their  nature,  it  is  advisable  to  avoid  using  the  word  "  fit," 
especially  if  we  are  discussing  symptoms  in  the  presence  of  the 
patient.  It  is  better  to  refer  simply  to  "  attacks."  Many 
epileptics  are  unaware  of  their  own  disease,  and  even  when  they 
know  its  nature,  they  dislike  hearing  about  their  "  fits." 

The  first  point  we  should  try  to  determine  is  whether  the 

65  E 


65  NERVOUS    DISEASES 

attacks  are  hysterical  or  epileptiform.  In  reference  to  this  the 
age  and  sex  of  the  patient  are  often  of  importance.  We  do  not 
meet  with  hysteria  in  infants,  and  rarely  in  children  below  the 
age  of  puberty.  Epilepsy  is  of  equal  frequency  in  both  sexes, 
whereas  hysteria  is  twenty  times  commoner  in  females  than  in 
males.  Hysterical  attacks  in  male  patients  are  most  frequent  in 
lads  at  about  the  age  of  puberty. 

Scheme  of  Investigation  in  Cases  of  Fits 

Exciting  cause.  Nature  of  warning,  if  any.  Onset,  sudden  or  gradual. 
Scream.  Injuries  during  falling.  Movements,  tonic,  clonic,  purposive. 
Starting-point  of  movements,  and  exact  order  of  spread.  Biting  of  tongue. 
Micturition  or  defsecation.  Colour  of  face,  pale,  flushed,  cyanosed.  Pupils. 
Conjunctival  reflexes.  Knee-jerks  immediately  after  attack.  Duration  of 
attack.     After-symptoms  (coma,  vomiting,  headache,  sleep,  &c.). 

Pursuing  the  foregoing  scheme,  we  should  inquire  whether 
there  was  any  apparent  cause  for  the  attack.  Hysterical  attacks 
generally  follow  some  emotional  disturbance.  Epilepsy  comes  on 
without  exciting  cause.  A  warning  or  aura  before  an  attack 
of  epilepsy  may  be  of  the  most  varied  character.  Perhaps 
the  commonest  is  the  "  epigastric "  aura,  or  there  may  be 
an  indescribable  feeling  of  terror,  subjective  auditory  or  visual 
phenomena  (visual  aurse  being  most  frequently  red  in  colour), 
unilateral  tingling  or  twitching  of  the  face  or  one  of  the  hmbs,  or 
a  "  dreamy  "  mental  state  (sometimes  associated  with  subjective 
sensations  of  smell  or  taste),  and  so  on,  according  to  the  particular 
cortical  area  whence  the  epileptic  explosion  happens  to  start.  But 
often  the  epileptic  has  no  aura  ;  he  falls  suddenly  as  if  struck 
down  by  an  unseen  hand.  If  we  happen  to  be  feehng  the  pulse 
of  an  epileptic  at  the  moment  of  onset  of  a  fit,  it  will  sometimes  be 
noticed  that  the  heart  suddenly  stops  for  a  few  seconds.  Suoh 
cardiac  arrest,  however,  is  not  invariable.  Hysterical  attacks 
usually  come  on  gradually,  and  are  often  preceded  by  the  hysteri- 
cal "  globus  "  or  ball  in  the  throat,  or  by  feelings  of  palpitation, 
excitement,  giddiness,  tingling  in  the  feet,  &c.  Sometimes  at  the 
onset  of  the  attack  the  epileptic,  as  he  falls,  utters  a  weird  epileptic 
cry  or  moan,  which  is  not  repeated.  By  this  time  he  is  already 
unconscious  and  does  not  hear  his  own  cry.     Frequently  he  injures 


FITS    AND    OTHER    CONVULSIVE    PHENOMENA     67 

himself  in  falling  especially  by  striking  his  head.  Many  chronic 
epileptics  may  be  recognised  by  the  presence  of  numerous  scars 
on  the  scalp  and  face.  The  hysterical  patient,  on  the  contrary, 
never  injures  herself  when  falhng.  She  comes  down  carefully, 
often  on  a  sofa  or  easy-chair.  She  not  uncommonly  screams,  and 
may  continue  to  scream  or  shout  throughout  the  attack. 

The  nature  of  the  movements  during  the  attack  is  of  importance. 
In  epilepsy  we  have  the  tonic  stage,  in  which  all  the  voluntary 
muscles,  including  those  of  respiration,  become  suddenly  rigid. 
The  patient,  therefore,  falls  like  a  log,  and  his  lips  and  face  become 
cyanosed,  his  pupils  dilating  and  becoming  insensitive  to  light. 
The  tonic  stage  passes  into  the  clonic,  in  which  violent  jerking 
occurs  in  all  the  voluntary  muscles,  at  first  rapid,  and  gradually 
becoming  slower  and  of  greater  range.  The  eyes,  which  during 
the  tonic  stage  have  been  drawn  to  one  side  (the  side  on  which 
the  tonic  spasm  was  more  intense),  now  show  rapid  clonic  jerks 
towards  that  side.  The  face  loses  its  cyanotic  hue,  air  re-enters 
the  lungs,  and  is  jerked  out  in  short  puffs  mixed  with  saliva, 
forming  a  froth  which  is  not  infrequently  blood-stained,  since  the 
jerking  tongue  may  be  bitten  by  the  clonic  movements  of  the  jaws. 
During  this  stage  the  patient  often  empties  the  bladder  and  some- 
times the  rectum.  Within  two  or  three  minutes  from  their 
onset  the  movements  gradually  cease,  and  the  patient  remains  in 
a  state  of  coma,  with  stertorous  breathing,  flaccid  Hmbs,  and 
sometimes  profuse  sweating,  the  eyes  being  now  turned  to  the 
side  opposite  to  that  towards  which  they  originally  deviated, 
and  the  pupils  being  now  contracted.  Then,  after  ten  minutes 
or  so,  the  coma  passes  off,  and  the  patient  may  vomit,  or  may 
wake  up,  perhaps  with  a  headache,  or  may  pass  into  a  sound  sleep. 

In  a  hysterical  attack,  on  the  other  hand,  the  patient's  face 
is  natural  in  colour,  never  cyanosed,  though  later  it  may  become 
flushed  from  physical  exertion.  The  voluntary  muscles  are  usually 
contracted,  the  fists  clenched,  the  eyes  tightly  closed  and  resistant 
to  opening,  but  if  the  eyes  be  forcibly  opened  the  eyeballs  roll 
upwards.  Then,  after  a  stage  of  general  tremor  totally  unhke  the 
clonic  stage  of  epilepsy,  the  patient  makes  violent  "  purposive  " 


68  NEEVOUS    DISEASES 

movements,  kicking,  pushing,  biting,  rolling  about,  banging  her 
head  on  the  floor,  beating  her  own  face,  pulling  her  hair,  &c. 
During  this  stage  various  grotesque  postures  may  be  assumed  ;  of 
these,  the  most  characteristic  is  one  in  which  the  back  is  arched 
(opisthotonos)  and  the  patient  rests  on  her  head  and  heels.  Or 
there  may  be  curving  of  the  trunk  laterally  (pleurosthotonos), 
or  forwards  (emprosthotonos),  "  crucifixion "  attitude,  &c.  The 
patient  may  talk,  scream,  or  sing  during  the  attack,  which  may  last 
for  many  minutes.  But  throughout  the  attack  the  pupils  generally 
react  to  Hght,  and  the  conjunctival  reflex  is  usually  preserved.  The 
hysterical  patient  never  bites  her  tongue,  though  she  may  bite  her 
lips  or  fingers,  or  snap  at  the  fingers  of  bystanders.  She  never 
empties  the  bladder  or  rectum  during  the  attack,  and  after  it  is 
over  she  may  or  may  not  have  any  recollection  of  what  has 
happened,  and  is  sometimes  in  a  semi-dazed  condition.  The 
hysterical  patient  is  more  likely  to  clear  up  suddenly  after  the 
fit  than  the  epileptic ;  also  she  is  more  likely  to  "  feel  better  " 
after  the  fit  than  in  the  case  of  an  epileptic. 

The  knee-jerks,  during  the  stage  of  flaccid  coma  terminating  a. 
severe  epileptic  fit,  may  be  temporarily  abolished,  but  soon  they 
become  exaggerated,  and,  for  a  few  minutes,  ankle-clonus  may 
often  be  ehcited,  and  the  plantar  reflex  may  be  extensor  in  type. 
In  hysteria  the  deep  reflexes  are  unaltered. 

If  we  bear  in  mind  the  foregoing  points,  the  diagnosis  between  a 
severe  epileptic  fit  and  an  attack  of  "grande  hysteric"  is  generally  easy. 

Catalepsy,  another  variety  of  hysterical  attack,  is  easily  recog- 
nised by  the  peculiar  immobility  of  the  limbs.  The  patient  during 
the  attack,  though  not  unconscious,  is  unable  to  move  a  muscle, 
but  her  limbs  are  plastic  like  those  of  a  lay  figure,  and  if  placed 
passively  in  any  posture,  remain  there. 

There  are  also  many  varieties  of  minor  hysterical  attacks,  easy 
of  recognition,  of  which  the  commonest  consist  merely  in  emotional 
outbursts  of  uncontrollable  laughing  or  crying,  or  a  feeling  of  a 
lump  in  the  throat — "  globus  hystericus  " — which  causes  the  patient 
to  swallow. 

Supposing,  then,  that  we  have  come  to  the  conclusion  that 


FITS    AND    OTHER    CONVULSIVE    PHENOMENA      69 

the  patient's  attacks  are  hysterical  and  not  epileptiform,  we  should 
not  rest  content  until  we  have  settled  the  further  point  as  to 
whether  the  hysterical  attack  was  preceded  by  an  attack  of 
minor  epilepsy  or  fetit  mal. 

Attacks  of  petit  mal  are  often  overlooked.  It  is  well  to 
remember  that  in  true  epilepsy  (whether  major  or  minor)  the  one 
essential  phenomenon  is  not  convulsions  but  loss  of  consciousness. 
In  petit  mal  it  may  be  the  only  phenomenon,  so  transient, 
perhaps,  that  the  patient  does  not  even  fall ;  he  simply  pauses 
for  an  instant  during  conversation,  looks  strange,  and  then  goes 
on  with  what  he  was  saying.  Or  he  may  fall  down  and  get 
up  again  immediately,  a  variety  of  epilepsy  which  is  often  mis- 
taken for  syncope,  but  is  distinguished  by  the  suddenness  of 
onset  and  of  recovery.  If  we  happen  to  observe  a  patient  at  the 
moment  of  his  attack  of  petit  mal,  we  generally  notice  that  the 
pupils  dilate  and  his  face  turns  momentarily  pale,  the  pallor  being 
followed  by  flushing.  It  is  immediately  after  such  a  minor  attack 
that  some  patients  go  on  to  a  post-epileptic  hysterical  attack,  and  if 
the  initial  epilepsy  be  not  recognised,  treatment  will  fail. 

Attacks  of  minor  epilepsy  are,  now  and  then,  associated  with 
post-epileptic  automatism,  in  which  the  patient  has  an  attack  of 
petit  mal  which  perhaps  passes  unnoticed  ;  he  then  proceeds  to 
perform  some  unusual  or  inappropriate  act,  of  which  he  has  no 
recollection  afterwards.  Perhaps  the  commonest  automatic  action 
is  that  of  undressing ;  or  he  may  proceed  to  empty  his  bladder,  as 
in  the  oft-quoted  instance  of  the  judge  who  did  so  in  the  corner  of 
his  court  of  justice  ;  or  he  may  perform  some  still  more  complicated 
action.  Thus  a  case  of  mine  was  that  of  a  well-known  financier 
who  had  several  attacks  of  loss  of  memory.  During  one  of  these, 
lasting  two  and  a  half  hours,  he  attended  an  important  board- 
meeting  and  proposed  certain  resolutions  to  which,  both  before 
and  after,  he  was  strongly  opposed.  He  then  took  a  friend  out  to 
lunch  and  returned  to  his  office.  He  finally  woke  up  and  asked 
his  confidential  clerk  where  he  had  been.  The  medico-legal  signi- 
ficance of  these  cases  is  of  importance,  since  such  a  patient,  in  a 
condition  of  post-epileptic  automatism,  may  commit  serious  and 


70  NERVOUS   DISEASES 

complicated  crimes,  of  whicli  he  has  afterwards  no  recollection. 
This  condition  is  sometimes  called  "  mashed  "  or  "  larval  "  epilepsy. 
It  is  possible  that  attaclvs  of  automatism  or  psychic  epilepsy  may 
occasionally  actually  replace  the  ordinary  epileptic  fit  without 
an  antecedent  attack  of  petit  mal,  may  in  fact  be  "  epileptic  equi- 
valents." But  the  more  carefully  such  cases  are  observed,  the 
oftener  is  some  indication  found  of  minor  epilepsy  immediately 
before  the  eccentric  action,  in  the  form  perhaps  of  initial  transient 
pallor.  This  was  so  in  the  case  of  the  financier  above  referred  to. 
Other  cases  of  ambulatory  automatism  are  hysterical  in  nature 
(see  later,  p.  378).  A  previous  history  of  epilepsy,  either  major  or 
minor,  is  of  great  diagnostic  value. 

Supposing  that,  having  excluded  hysteria,  we  arrive  at  the 
conclusion  that  a  patient's  fits  are  epileptiform,  we  must  still  re- 
member that  other  conditions  besides  idiopathic  epilepsy  can  pro- 
duce epileptiform  fits.  Sudden  obstruction  of  the  larynx,  e.g.  by 
a  piece  of  meat,  bolted  in  a  hurry,  becoming  impacted  at  the  top 
of  the  larynx,  may  cause  immediate  unconsciousness  followed  by 
a  typical  epileptiform  fit  and  by  death  unless  the  offending  foreign 
body  be  promptly  extracted.  Similar  asphyxial  fits  sometimes 
occur  in  cases  of  attempted  suicide  by  hanging,  where  the  uncon- 
scious person  is  cut  down  in  time.  Fits  may  also  be  of  toxic 
origin.  Acute  alcoholic  or  absinthe  poisoning  may  produce  coma 
and  convulsions.  The  history  and  the  smell  of  the  breath  will 
usually  guide  us  in  such  cases.  The  sudden  withdrawal  of 
alcohol  from  a  chronic  drunkard  is  sometimes  followed  by  an 
epileptiform  fit.  In  patients  suffering  from  the  convulsions  of 
lead  jJoisoning  there  are  usually  other  signs  of  plumbism,  such  as 
the  blue  hne  in  the  gums,  high  arterial  tension,  weakness  of  the 
extensors  of  the  wrist,  optic  neuritis.  Toxuis  produced  within  the 
body  may  also  cause  fits  exactly  sunilar  to  epilepsy,  witness  the 
urcemic  convulsions  of  Bright 's  disease  and  of  pvierperal  eclampsia. 
In  every  case  of  fits  appearing  in  a  previously  healthy  individual, 
the  urine  should  be  tested  and  the  optic  discs  examined.  In  the 
case  of  a  young  officer  who  was  brought  into  hospital  at 
Pretoria  suffering  from  a  succession  of  fits  typically  epileptic   in 


FITS    AND    OTHER    CONVULSIVE    PHENOMENA     71 

character,  acute  nephritis  was  the  cause.  In  chronic  renal 
disease,  besides  the  cardio-vascular  changes,  there  not  uncommonly 
exists  albuminuric  retinitis,  which  is  of  great  diagnostic  significance. 
When  we  come  to  the  subject  of  infantile  convulsions  we  shall  find 
that  many  of  them  are  toxic  in  origin. 

Epileptiform  fits  may  occur  during  the  course  of  general  paralysis 
of  the  insane  ;  they  may,  in  fact,  be  the  first  symptom  of  the 
disease.  Epileptic  fits  appearing  for  the  first  time  in  a  middle- 
aged  patient  should  always  suggest  the  possibility  of  paralytic 
dementia.  In  such  cases  we  look  for  inequality  or  irregularity  of 
the  pupils,  and  especially  loss  of  the  light  reflex,  mental  changes, 
facial  tremors,  and  slurring  articulat'on,  and  a  history  of  syphilis 
should  be  sought.  Lumbar  puncture  may  show  lymphocytosis 
of  the  cerebro-spinal  fluid,  a  condition  which  is  constant  in  general 
paralysis  but  does  not  occur  in  idiopathic  epilepsy. 

Epileptiform  or  hystero-epileptiform  fits  may  also  occur  in 
psycJiasthenic  individuals.  Such  patients  have  stigmata  of  psych- 
asthenia  in  the  form  of  phobias,  tics,  obsessions,  &c.  (see  p.  358). 
Epileptiform  fits  in  psychasthenia,  unlike  true  epilepsy,  occur  only 
after  some  direct  exciting  cause,  such  as  physical  or  mental  over- 
exertion, excitement,  &c.  The  attacks,  as  a  rule,  are  few  in  number 
and  may  be  limited  to  a  single  one. 

Intra-cranial  tumours  anywhere,  even  deep  within  the  substance 
of  the  brain,  may  cause  general  epileptiform  fits,  from  increased 
intra-cranial  pressure.  Here  we  are  usually  guided  by  the  cardinal 
signs  of  intra-cranial  tumour — ^headache,  vomiting,  optic  neuritis,  &c. 

All  the  epileptiform  fits  to  which  we  have  as  yet  alluded  have 
a  bilateral  general  distribution,  and  are  not  succeeded  by  any 
localised  paralysis.  But  when  fits  are  produced  by  gross  focal  irrita- 
tion of  the  cortex  their  onset  is  a  local  one,  and  they  are  not 
necessarily  associated  with  loss  of  consciousness.  Such  "  JacJc- 
sonian  "  fits  are  usually  followed  by  weakness  of  the  part  which 
is  primarily  convulsed.  Jacksonian  fits  may  occur  as  often  as 
fifty  or  a  hundred  times  a  day.  They  usually  begin  with  a 
subjective  sensory  aura,  such  as  tingling,  numbness  or  twitching, 
localised  in  some  particular  part,  e.g.  the  thumb  or  big  toe.     Then 


72  NEKVOUS    DISEASES 

there  is  tonic  spasra  of  that  part,  followed  by  clonic  jerking. 
This  may  remain  conjEined  to  the  muscles  where  it  began,  or 
it  may  spread  to  others.  If  it  spreads,  it  does  so  by  a 
deliberate  march  from  one  cortical  centre  to  another  (Fig.  3,  p.  5). 
Thus  a  fit  commencing  in  the  big  toe  would  occur  successively 
in  the  ankle,  knee,  hip,  shoulder,  elbow,  hand,  &c.,  and  would 
af?ect  the  face  last  of  all.  Or  a  fit  beginning  in  the  elbow  would 
spread  via  the  shoulder,  hip  and  knee,  to  the  toes,  and  simul- 
taneously via  the  wrist,  fingers  and  neck,  to  the  face  and  tongue, 
as    the  ripples  produced  by  dropping  a  stone  into  a  pool  spread 


h-lG.  31.  1''I6.  32. 

Cortical  gumma  of  the  face-centre  of  the  right  cerebral  cortex. 

Fig.  SI  shows  patient  during  a  Jacksonian  fit  of  the  left  face. 
Fig.  32  shows  wealfness  of  the  left  face  on  voluntary  movement. 

in  ever- widening  circles.  A  patient  who  has  Jacksonian  fits 
may  remain  conscious  throughout  the  fit  and  may  even  be  able 
to  speak,  though  he  is  usually  somewhat  confused  and  excited. 
But  if  the  convulsion  spreads  to  the  opposite  cortical  area,  thus 
becoming  bilateral,  consciousness  is  lost  as  the  fit  crosses  over, 
Jacksonian  fits  are  followed  by  local  weakness  and  increased  deep 
reflexes  in  the  convulsed  part.  Fig.  31  shows  a  patient  during 
a  locahsed  fit  in  the  left  face,  due  to  a  gumma  in  the  cortical  facial 
centre.  Fig.  32  shows  the  maximum  voluntary  movement  of  the 
face  after  an  attack.  It  will  be  seen  that  the  left  lower  face 
is  markedly    weaker    than    the    right.      The    localised    paralysis 


FITS    AND    OTHER    CONVULSIVE    PHENOMENA     73 

passes  off  in  the  reverse  order  from  that  in  which  the  spasm 
appeared,  the  muscles  first  convulsed  being  the  last  to  recover 
power. 

Of  course,  cortical  lesions  will  produce  locahsed  motor  pheno- 
mena only  if  they  aflect  the  motor  centres  in  the  region  of  the 
pre-central  gyrus.  A  focal  lesion  of  a  sensory  cortical  area  pro- 
duces, not  a  motor,  but  a  sensory  -fit.  Thus  disease  of  the  tip 
of  the  temporal  lobe  (Fig.  4,  p.  5)  causes  a  sudden  subjective 
sensation  of  smell  or  taste  (often  associated  with  a  characteristic 
"  dreamy  "  mental  state),  occipital  lesions  cause  subjective  visual 
hallucinations  such  as  flashes  of  light,  and  so  on.  Moreover,  after 
the  sensory  fit  it  is  not  uncommon  to  find  temporary  sensory 
paralysis,  e.g.  anosmia  after  a  temporal  fit,  or  hemianopia  after 
an  occipital  fit. 

A  Jacksonian  fit,  of  whatever  variety,  is  the  result  of  a  local 
lesion  in  the  neighbourhood  either  of  the  cortex  or  of  its  superjacent 
meninges  or  bones.  If  the  lesion  be  in  the  substance  of  the  cortex, 
not  merely  superficial  to  it,  there  is  often  some  local  paralysis  even 
before  the  fit  occurs. 

Locahsed  fits  may  be  produced  by  any  irritative  cortical  lesion. 
The  commonest  causes  are  tumours,  syphihtic  or  otherwise,  ab- 
scesses, meningitis  of  any  variety,  local  haemorrhages,  depressed 
fractures,  and  so  on.  Localised  fits  may  also  be  produced  by 
sub-cortical  tumours  in  the  pre-central  region.  In  such  cases 
we  observe  muscular  paresis  in  the  affected  limb,  together  with 
recurring  convulsive  phenomena  in  the  limb  ;  but  the  point  of 
onset  of  the  successive  fits  is  less  constant  than  in  a  true  cortical 
convulsion,  and  the  fit  begins  sometimes  in  one,  sometimes  in 
another  muscle-group  of  the  affected  limb.-^  We  should  also  bear 
in  mind  that  Jacksonian  fits  may  occur  in  certain  cases  of  general 
paralysis  of  the  insane,  and  sometimes  even  in  ursemia. 

Infantile  Convulsions  are  epileptiform  attacks  occurring  in 
infancy.  The  symptoms  are  similar  to  those  of  true  epilepsy,  but 
less  violent.  When  called  to  see  a  child  with  convulsions,  we 
should  first   examine  for   rickets,   since    rickety   and   hereditarily 

^   Of.  van  Valkenburg,  Neurologisches  Centralhlatt,  1906,  p.  594. 


74  NERVOUS    DISEASES 

neurotic  children  are  especially  prone  to  convulsions.  We  should 
also  try  to  determine  whether  the  fits  are  reflex,  toxic,  or  organic 
in  origin.  In  rickety  infants  of  neurotic  inheritance  reflex  con- 
vulsions may  be  set  up  by  peripheral  irritation  such  as  the  cutting 
of  a  tooth,  round-worms  in  the  intestine  (thread-worms  do  not 
cause  convulsions),  a  tight  prepuce,  &c.  Moreover,  rickety  children 
often  have  other  nervous  symptoms,  such  as  tetany,  laryngismus 
stridulus,  and  the  well-known  inversion  of  the  thumbs  towards 
the  palms,  a  phenomenon  which  sometimes  precedes  a  convulsion. 
Toxic  conditions  may  produce  convulsions  in  previously  healthy 
children.  Thus  any  acute  fever  such  as  pneumonia,  measles,  scarlet 
fever  or  influenza,  may  be  ushered  in  by  a  convulsion  instead  of 
by  a  rigor  as  in  the  adult.  The  convulsions  produced  by  round- 
worms may  be  partly  toxic  in  origin.  Uraemic  convulsions  occur 
in  children,  though  less  often  than  in  adults,  and  in  cases  with 
recurring  convulsions  the  urine  should  always  be  examined. 
Asphyxial  convulsions,  due  to  deficient  oxygenation  of  the  brain, 
occur  in  dyspnoea  from  any  cause,  e.g.  during  pneumonia  and 
diphtheria,  during  a  paroxysm  of  whooping-cough,  or  in  the 
cyanosis  of  congenital  heart  disease.  Intra-cranial  organic,  lesions 
may  cause  infantile  convulsions.  Thus,  for  example,  poHo-ence- 
phalitis  superior,  an  acute  inflammatory  afiection  of  the  cortex, 
has  a  febrile  onset  with  vomiting  and  convulsions,  usually  more 
marked  on  one  side  than  on  the  other.  After  the  convulsions 
have  passed  off,  the  child  is  often  left  permanently  hemiplegic  or 
diplegic.  If  the  cortex  of  the  frontal  region  is  afiected,  permanent 
mental  dulness  may  remain.  Local  disease  or  injury  of  the  bones 
or  membranes  may  produce  infantile  convulsions.  Convulsions 
appearing  within  a  few  hours  after  birth  are  not  unfrequently  the 
result  of  compression  of  the  brain  by  a  meningeal  haemorrhage. 
Meningitis,  whether  due  to  the  tubercle  bacillus,  to  syphiHs,  or 
to  other  organisms,  may  produce  convulsions,  not  only  when 
cortical,  in  which  case  convulsions  appear  early,  but  also  in 
basal  cases,  where  the  fits  are  due  to  increased  intra-cranial 
pressure. 

Epileptiform  fits  also  occur  in  one  variety  of  the  Stokes-Adams' 


FITS    AND    OTHER    CONVULSIVE    PHENOMENA     75 

syndrome,  a  condition  which  occurs  after  middle  Hfe,  usually  in 
male  patients  with  degenerate  arteries,  and  is  characterised 
by  paroxysmal  attacks  of  abnormal  slowness  of  the  ventricular 
beat,  the  rate  sinking  as  low  as  twenty  per  minute  or  even  less, 
together  with  excessive  pulsation  in  the  veins  at  the  root  of  the 
neck,  more  rapid  than  the  ventricular  beats,  and  corresponding 
with  the  auricular  contractions.  Such  a  patient  is  liable  to 
syncopal  attacks,  to  which  may  be  superadded  epileptiform  fits 
or  attacks  of  coma  without  convulsions.  Fits  do  not  occur  unless 
the  heart-block  is  complete,  where  the  ventricle  no  longer  responds 
to  auricular  stimulation.  More  or  less  slowness  of  pulse  usually 
persists  between  the  paroxysms,  as  a  permanent  phenomenon. 
The  condition  is  frequently  due  to  disease,  syphilitic  or  otherwise, 
of  the  auriculo-ventricular  muscle-bundle  of  Stanley  Kent  -^  and 
His,  which  arises  in  the  right  auricle,  traverses  the  inter-ventri- 
cular septum  and  is  distributed  to  both  ventricles.  When  this 
bridge  is  diseased,  the  normal  stimulus  from  auricle  to  ventricle 
is  delayed  or  may  even  be  completely  blocked.  This  is  known 
as  heart-block,  in  which  the  auricles  go  on  contracting  normally, 
but  the  ventricle  only  responds  to  every  second  or  every  third 
stimulus.  There  is  thus  a  dissociation  between  auricular  and 
ventricular  rhythm.^ 

Strychnine  Convulsions  should  never  be  confounded  with 
epileptiform  fits,  since  they  begin  with  clonic  spasms,  and 
shortly  become  tonic  with  opisthotonos,  the  tonic  spasms  recurring 
again  and  again  with  increasing  severity.  A  patient  poisoned  by 
strychnine  is  not  unconscious.  Moreover,  there  are  periods  of 
intermission,  lasting  for  several  minutes  at  a  time,  during  which 
the  muscles  are  relaxed.  The  tonic  spasms  of  tetanus  might  be 
mistaken  for  strychnine-poisoning,  but  they  have  no  initial  clonic 
stage.  The  earliest  symptom  of  tetanus  is  the  well-known  tonic 
spasm  of  the  jaw  muscles,  producing  "  lock-jaw."  To  this  there 
are  superadded  paroxysms  of  tonic  spasm  in  the  face  {risus 
sardonicus),  trunk  and  limbs,    with  opisthotonos,  somewhat  like 

^   Kent,  Journal  of  Physiology,  1S93,  vol.  xiv.  p.  233. 
-  Mackenzie,  Diseases  of  the  Heart,  1908,  p.  169. 


76 


NEEVOUS   DISEASES 


those  of  the  tonic  stage  of  strychnine-poisoning.  Between  the 
tetanic  paroxysms  there  is  no  complete  muscular  relaxation  as 
in  strychnine-poisoning,  but  simply  a  remission  in  the  degree  of 
spasm,  the  jaw  muscles  remaining  partially  contracted. 

A  patient  suffering  from  rabies  exhibits  great  mental  excite- 
ment, with  tonic  spasm  of  the  muscles  of  deglutition,  especially  on 
attempting  to  swallow  liquids  (hence  the  misnomer  hydrophobia). 


Fig.  33.— Tetany. 

The  spasm  may  also  be  induced  by  other  stimuli  such  as  a  bright 
light  or  a  loud  sound.  The  spasm  spreads  to  other  muscles, 
especially  those  of  respiration,  and  severe  opisthotonos  may  super- 
vene at  the  end,  the  patient  dying  either  of  respiratory  spasm 
or  from  syncope.  Hydrophobia  may  be  simulated  by  hysterical 
patients  who  have  been  bitten  by  a  non-rabid  dog,  and  in 
such  cases  globus  hystericus  and  hysterical  opisthotonos 
may  both  occur,  but  true  respiratory  spasm  does  not  occur  in 


FITS    AND    OTHER    CONVULSIVE    PHENOMENA      77 

hysterical  attacks,  though   there   may   be   hysterical  rapidity  of 
breathing. 

During  an  attack  of  tetany  the  posture  is  very  characteristic. 
There  is  a  bilateral  tonic  spasm,  usually  painful,  of  the  hands  and 
feet,  the  hand  assuming  a  conical  shape  ("  main  d'accoucheur  "),  the 
fingers  being  extended  at  the  inter-phalangeal  joints,  slightly  flexed  at 
the  metacarpo-phalangeal  joints  and  pressed  together  with  the  thumb 
usually  tucked  inside  the  fingers  ;  at  the  same  time  the  muscles  of  the 
thenar  and  hjrpothenar  eminences  are  contracted,  so  that  the  hollow 
of  the  palm  is  deepened.  In  the  feet,  the  toes  are  flexed  towards  the 
sole,  the  ankle  is  dorsiflexed  and  the  foot  is  sometimes  inverted. 
These  postures  may  persist  during  sleep.  Pressure  on  the  nerve- 
trunks  of  the  affected  limb  induces  a  typical  spasm  (Trousseau's 
sign),  and  the  muscles  and  nerves  are  unduly  irritable  both  to  fara- 
dism  and  to  galvanism  (Erb's  sign).  Tetany  is  most  commonly  met 
with  in  rickety  children  (Fig.  33),  in  whom  it  is  often  associated 
with  laryngismus  stridulus  and  with  excessive  irritability  on  per- 
cussion of  the  facial  nerve  (Chvostek's  sign).  But  it  occasionally 
occurs  in  adults,  e.g.  after  extirpation  of  the  thyroid  gland,  or 
rather  of  the  parathyroids.  The  parathyroid  glands  produce  an 
internal  secretion  which  neutralises  certain  toxic  products  of 
metabolism.  Tetany  is,  therefore,  sometimes  a  symptom  of 
parathyroid  deficiency,  whether  arising  from  disease  or  from 
artificial  removal  of  the  gland.  Tetany  also  occurs  sometimes 
during  pregnancy  or  lactation,  and  as  a  grave  terminal  symptom 
in  dilatation  of  the  stomach.  This  variety  of  tetany  is  probably 
toxic  in  origin  :  so  also  are  the  rare  cases  of  tetany  associated  with 
congenital  dilatation  of  the  large  intestine  in  children.^  Cataract 
is  a  curiously  frequent  concomitant  of  the  gastric  form  of  tetany. 
An  endemic  form  of  tetany  also  occurs  in  certain  Continental 
towns,  chiefly  in  the  winter  months.  It  is  especially  common 
amongst  shoemakers. 

Cerebellar  Fits. — Irritative  lesions  of  the  cerebellum  are 
occasionally  associated  with  cerebellar  fits.  These  are  never  clonic, 
but  consist  of  tonic  spasms,  sudden  in  onset.     In  unilateral  cere- 

^  Langmead,  Lancet,  Jan.  19,  1907. 


78  NERVOUS    DISEASES 

bellar  disease  tlie  spasms  are  more  marked  in  the  ipso -lateral 
limbs  than  in  those  of  the  opposite  side.  The  face  is  usually- 
unaffected.  The  ipso-lateral  limbs  become  rigidly  adducted  to 
the  trunk,  the  contra-lateral  limbs  are  abducted,  whilst  at  the 
same  time  there  is  a  screw-like  rotation  of  the  limbs,  trunk  and 
head  around  their  own  long  axes,  from  the  side  of  the  lesion 
towards  the  healthy  side,^  and  a  deviation  of  the  eyes  towards 
the  healthy  side.  Hughlings  Jackson  has  described  another  variety 
of  cerebellar  fit  occurring  in  cases  of  tumour  of  the  middle  lobe. 
Here  also,  as  in  tumours  of  the  lateral  lobe,  the  fits  are  tonic,  not 
clonic.  They  consist  of  head-retraction  with  arching  of  the  back, 
flexion  of  the  elbows,  supination  of  the  hands,  and  rigid  extension 
of  the  legs,  with  pointing  of  the  toes. 

But  let  us  not  forget  that  epileptiform  fits,  cerebral  in  type, 
may  also  occur  in  cerebellar  tumours,  due  either  to  the  general 
increase  of  intra-cranial  pressure,  or  to  a  fulminating  meningitis 
superadded  to  an  old  tuberculous  tumour. 

^   Grainger  Stewart  and  Holmes/Brflm,  1904. 


CHAPTER   VI 

INVOLUNTARY   MOVEMENTS 

Besides  fits,  which,  we  have  already  considered,  there  are  many 
other  conditions  in  which  involuntary  contractions  occur  in 
the  voluntary  muscles.  But  our  knowledge  of  the  mechanism 
of  their  causation  is  so  incomplete  that  it  is  impossible 
at  present  to  classify  them  accurately.  We  must  therefore 
content  ourselves,  in  the  meanwhile,  with  referring  to  some  of 
their  chief  clinical  varieties. 

In  studying  involuntary  movements  occurring  in  striated 
muscles,  it  is  important  to  observe  whether  the  movement  is  con- 
fined to  an  individual  muscle  or  part  of  a  muscle,  or  whether,  on 
the  other  hand,  it  consists  in  alternate  contraction  of  muscles  and 
of  their  antagonists.  We  should  also  observe  whether  the  abnormal 
muscular  contractions  produce  movements  of  a  joint,  or  whether 
they  are  so  localised,  either  to  a  small  muscle  or  to  part  of  a 
larger  one,  that  we  merely  see  or  feel  the  muscle  fibres  contracting 
beneath  the  skin. 

The  muscular  phenomenon  known  as  shivering  or  rigor  is  some- 
times physiological.  For  example,  when  a  healthy  person  becomes 
chilled,  as  by  prolonged  swimming,  he  often  shivers  on  coming 
out  of  the  water.  The  involuntary  muscular  contractions  of 
which  shivering  consists  are  for  the  purpose  of  producing  heat 
and  thereby  raising  the  depressed  body-temperature.  But  often 
rigors  are  toxic  in  origin,  as  are  those  occurring  at  the  onset  of 
certain  acute  fevers.  Thus  we  have  rigors  in  pneumonia,  ague, 
influenza,  scarlet  fever,  &c.  And  the  rigor  which  sometimes  follows 
catheterisation  is  probably  also  toxic  in  origin,  since  it  rarely  occurs 
except  when  there  is  a  raw  surface  in  a  urinary  tract  which  is  not 
aseptic.  In  all  these  toxic  rigors,  although  the  shivering  patient 
has  a  sensation  of  cold,  his  tsmperature  meanwhile  is  rising, 
and  it  continues  to  rise  until  the  rigor  stops.     He  has  the  sensa- 


80  ■  NEEVOUS  DISEASES 

tion  of  cold  because  by  vasomotor  action  the  blood  is  driven  out 
of  his  skin,  which  is  therefore  cooled  and  is  actually  cold,  although 
the  temperature  of  the  blood  is  raised. 

Transient  flickering  or  quivering  of  a  muscle,  a  condition  known 
as  myokymia  (or  more  popularly  as  "  live  flesh  "),  affecting  a  few 
muscle-bundles  of  a  single  muscle,  without  producing  movement 
of  a  joint,  is  not  uncommon  in  people  who  are  anaemic  or 
out  of  health.  It  is  specially  common  in  the  orbicularis  oculi 
and  in  some  of  the  larger  muscles  of  the  limbs,  e.g.  the  deltoid  and 
biceps  in  the  upper  limb,  the  glutei  and  quadriceps  in  the  lower. 
This  variety  of  myokymia  is  not  associated  with  muscular  atrophy, 
nor  with  any  alteration  of  electrical  excitability.  It  is  unaffected 
by  rest  or  by  voluntary  exertion,  and  has  no  serious  significance. 

Sometimes,  however,  fibrillary  movement  occurs  in  organic 
lesions  of  the  lower  motor  neurone.  Thus  in  the  muscular  atrophy 
of  chronic  anterior  'poliomyelitis,  of  amyotrophic  lateral  sclerosis,  and 
of  some  cases  of  syringomyelia,  diseases  in  which  the  cells  of  the 
anterior  cornua  are  undergoing  slow  degeneration,  there  may  be  seen 
fibrillary  or  fascicular  tremors  in  the  wasting  muscles.  This 
quivering  myokymia  can  often  be  elicited  by  gentle  flicking,  or  by 
a  breath  of  cold  air  blown  over  the  skin.  A  precisely  similar 
fibrillary  tremor  occurs  in  the  wasting  tongue  of  bulbar  paralysis, 
when  the  degenerative  process  has  involved  the  h5^oglossal 
nuclei.  Fibrillary  tremor  does  not  occur  in  the  primary 
myopathies,  whether  atrophic  or  pseudo-hypertrophic  in  type. 
In  other  cases  fibrillary  tremor  occurs  in  the  distribution  of  a 
motor  nerve  which  has  begun  to  recover  from  previous  paralysis. 
It  is  not  uncommon  in  the  face  during  convalescence  from  facial 
palsy,  and  sometimes  it  persists  for  months  and  years  after 
voluntary  power  has  returned,  as  in  the  case  of  a  professional 
friend  of  my  own  who  is  otherwise  perfectly  well.  More  usually 
the  myokymia  passes  off  when  motor  power  has  been  restored. 

Somewhat  different  in  appearance  is  the  condition  known 
as  myoclonus,  a  rare  disease,  characterised  by  paroxysms  of 
sudden  shock-like  contractions  in  various  muscles,  lasting  for 
several  minutes  at  a  time,  irregular  in  rhythm  and  varying  in 


INVOLUNTARY    MOVEMENTS 


81 


rapidity  from  ten  to  fifty  per  minute.  In  slight  cases  the  twitches 
may  be  insufl&cient  to  produce  movements  in  the  affected  parts. 
The  muscles  affected  are  usually  those  of  the  limbs,  especially  the 
lower  limbs,  often  symmetrically  on  the  two  sides,  but  contractions 
may  also  occur  in  the  trunk  and  even  in  the  face.     Sometimes  the 


Fig.  34. — Unverricht's  family  myoclonus  or  "myoclonus  epilepticus"  in  a  boy 
aged  13.  Besides  the  muscles  indicated  by  shading  in  the  diagram,  the  soft 
palate  was  also  affected. 

diaphragm  and  the  larynx  are  affected,  so  that  curious  grunting 
respiratory  sounds  are  produced.  There  is  no  muscular  atrophy 
or  alteration  in  electrical  excitability.  The  spasms  cease  during 
sleep.  Several  varieties  of  myoclonus  have  been  observed ;  in 
one — Friedreich's  paramyoclonus  multiplex,  usually  a  disease  of 
adult    life  —  the     myoclonus    ceases    on    voluntary    movement. 


82 


NEKVOUS    DISEASES 


Another  yariety  is  Unverriclit's  family  myoclonus  or  myoclonus 
epilepticus,  in  which  several  members  of  a  family  are  affected,  all 
belonging  to  the  same  generation,  though  the  disease  is  not  handed 
down  from  parent  to  child.  In  addition  to  the  myoclonus,  these 
patients  have  epileptiform  fits,  and  they  tend  ultimately  to  become 
more  or  less  demented.    Moreover,  the  muscular  contractions  in 


Fjg.  35. — Friedreich's  paiamyoclonus  multiplex  in  a  tnan  aged  50  (the  affected 
muscles  are  indicated  by  shading). 

family  myoclonus  are  intensified  by  voluntary  movement  and  by 
psychical  excitement.  Family  myoclonus  usually  manifests  itself 
in  early  life,  often  at  or  before  puberty.  Thus  in  a  little  boy  of 
thirteen  suffering  from  myoclonus  affecting  the  muscles  of  the  neck, 
shoulders,  trunk,  thighs  and  cremasters  (see  Fig.  34),  the  condition 
had  existed  since  the  age  of  four,  and  he  had  also  epileptiform 
fits.     Two  elder  brothers  were  similarly  affected,  both  of  whom, 


INVOLUNTARY    MOVEMENTS  83 

as  the  patient  graphically  put  it,  began  to  "  click  "  at  the  age 
of  seven.  On  the  other  hand,  another  patient  suffering  from 
Friedreich's  paramyoclonus  showed  no  symptoms  of  the  disease 
till  the  age  of  forty-seven.  He  never  had  fits,  and  at  the  age  of 
fifty,  when  he  came  under  observation,  he  had  myoclonic  shocks 
limited  to  the  muscles  indicated  in  the  accompanying  diagram 
(Fig.  35).  Another  variety  is  the  nystagmus -myoclonus  of  Lenoble 
and  Aubineau,  to  which  we  shall  refer  later  (see  p.  134). 

We  next  pass  to  the  consideration  of  tremors.  The  term  "tremor'' 
is  applied  to  involuntary  rhythmic  oscillations  of  one  or  more  parts 
of  the  body,  resulting  from  the  alternate  contraction  of  muscle- 
groups  and  of  their  antagonists.  A  simple  tremor  is  one  which 
affects  a  single  muscle-group  and  its  antagonists,  whilst  in  a  com- 
pound tremor  several  groups  with  their  antagonists  are  in  action, 
producing  a  complex  movement,  e.g.  flexion  and  extension  of  the 
fingers  combined  with  pronation  and  supination  of  the  forearm. 
Tremors  may  be  rapid  or  slow  ;  they  may  be  diminished  or  increased 
by  voluntary  exertion,  and  they  generally  cease  during  sleep. 

We  must  not  forget  that  an  ordinary  voluntary  muscular 
movement  is  not  the  result  of  a  continuous  muscular  contraction, 
but  is  constituted  by  the  fusion  of  a  rapid  succession  of  short  single 
contractions,  averaging  from  ten  to  twelve  per  second.  In  condi- 
tions of  temporary  fatigue  or  of  chronic  asthenia  the  rate  of  these 
muscle  discharges  becomes  slower  and  less  regular,  so  that  the 
individual  muscular  contractions  fuse  less  perfectly  and  the  result 
is  a  very  fine  tremor.  In  emotional  excitement — more  often  in 
states  of  fear  than  from  pleasurable  emotion — there  may  be 
a  fine  rhythmic  tremor  of  about  eight  or  nine  oscillations  per 
second,  familiar  to  the  knees  of  many  a  public  speaker.  The 
same  occurs  in  exojjhthalmic  goitre.  This  tremor  is  made  more 
apparent  by  voluntary  exertion.  It  is  best  elicited  by  making  the 
patient  hold  his  hands  horizontally  in  front  of  him,  with  the 
fingers  widely  spread.  We  can  then  feel  the  tremor  even  better 
than  see  it,  by  placing  our  own  fingers  lightly  on  the  dorsum  of  the 
patient's  hand.  This  fine  tremor  affects  all  the  limbs,  and  in 
many  cases  can  be  detected  by  simply  placing  one's  hand  on  the 
patient's  shoulder. 


84  NERVOUS    DISEASES 

Similar  fine  tremors  also  occur  in  certain  toxic  conditions.  The 
tremor  of  chronic  alcoholic  poisoning  is  famiHar  to  the  lay  observer, 
and  when  an  alcoholic  patient  becomes  dehrious  and  maniacal, 
his  tremors  are  so  evident  that  the  condition  is  termed  "  dehrium 
tremens."  But  other  poisons  besides  alcohol  produce  fine 
tremors  :  for  example,  nicotine  poisoning  from  excessive  cigarette- 
smoking,  also  chronic  poisoning  by  lead,  mercury,  chloral,  cocaine, 
tea,  coffee,  tobacco,  &c. 

In  cases  of  suspected  alcoholism  a  valuable  corroborative  sign, 
known  as  Quinquaud's  finger-crepitation,  may  often  be  elicited.  In 
testing  for  this,  we  make  the  patient  extend  the  fingers  at  the  inter- 
phalangeal  joints  and  press  them  at  right  angles  to  the  palm  of  our 
own  hand,  which  we  hold  in  a  vertical  position.  For  the  first  two 
or  three  seconds  nothing  particular  is  noticed,  but  if  the  patient 
be  a  chronic  alcoholic,  we  soon  begin  to  feel  a  series  of  slight 
shocks,  as  if  the  phalanges  of  each  finger  were  knocking,  one 
against  the  other,  trying  to  reach  our  palm. 

The  tremor  of  paralysis  agitans  occurs  at  rest  and  is  generally 
rather  coarse,  varying  in  different  cases  from  four  to  seven  oscilla- 
tions per  second.  It  produces  joint  movements,  e.g.  the  well-known 
"  pill-rolling  "  movement  of  the  thumb  and  fingers,  flexion-extension 
movement  of  the  wrists,  pronation- supination  of  the  forearm,  flexion- 
extension  of  the  ankle,  &c.  The  coarser  the  movement,  the  slower 
is  the  rhythm.  Paralysis  agitans  generally  begins  unilaterally,  and 
may  remain  confined  to  one  side  for  some  time  before  ultimately  be- 
coming bilateral,  as  may  be  seen  in  Figs.  36  and  37,  which  are  taken 
from  the  same  patient  at  an  interval  of  three  years.  Usually  the 
tremor  of  paralysis  agitans  can  be  temporarily  controlled  by 
voluntary  exertion.  But  this  is  not  always  so  ;  indeed,  cases  occur  in 
which  voluntary  movement  increases  the  tremor.  Paralysis  agitans 
is  always  accompanied  by  rigidity  in  the  affected  muscles ;  in 
fact,  rigidity  may  be  well  marked  without  tremor,  in  the  so-called 
"  paralysis  agitans  sine  agitatione."  An  attack  of  ordinary 
hemiplegia  occurring  in  a  patient  with  paralysis  agitans  arrests 
the  tremor  in  the  hemiplegic  limbs,  but  if  the  hemiplegia  be  not 
complete  or  permanent,  the  tremor  may  subsequently  reappear. 

Senile  tremor  is  not  unhke  the  tremor   of  paralysis  agitans, 


INVOLUNTARY   MOVEMENTS  85 

but  its  onset  occurs  much  later  in  life.  Moreover,  it  begins 
bilaterally,  especially  in  the  head,  jaw,  and  lips,  and  is  unaccom- 
panied by  the  characteristic  rigidity  of  Parkinson's  disease. 
Thus  in  a  famous  old  admiral  it  began  at  the  age  of  eighty-four 
as  a  gentle  antero-posterior  tremor  of  the  tongue,  with  a  syn- 
chronous movement  of  the  orbicularis  oris.  Both  his  hands  had 
tremor  and  an  interosseal  attitude  like  that  of  paralysis  agitans, 
but  without  rigidity. 


■5»  *» 


V  -    *«.. 


Fig.  36.— Paralysis  Agitans,  Fig.  37.— Paralysis  Agitans  :— 

left-sided.  the  same  patient  as  in  Fig. 36, 

three  years  later. 

In  rickety  children,  especially  during  the  second  six  months 
after  birth,  we  sometimes  observe  a  peculiar  involuntary  rotatory 
or  nodding  tremor  of  the  head  which  usually  comes  on  quite 
suddenly  in  winter-time  and  is  known  as  spasmus  nutans.  It 
is  generally  accompanied  by  fine,  rapid  nystagmus,  which  may  be 
more  marked  in  one  eye  than  in  the  other.  If  we  fix  the  child's 
head,  the  nystagmus  increases.  The  head  movement  is  more  often 
a  lateral  rotation  than  an  antero-posterior  nodding.  It  stops  when 
the  child's  eyes  are  closed,  either  voluntarily  or  artificially.     The 


86  NERVOUS    DISEASES 

symptom  persists  for  six  or  eight  weeks  or  longer,  and  then  passes 
off,  perhaps  to  return  again  in  the  following  winter.  It  is  not 
associated  with  any  mental  defect. 

Head-rolling  is  another  variety  of  involuntary  rhythmic  move- 
ment met  with  in  children,  chiefly  below  the  age  of  two  years. 
Many  of  the  patients  are  rickety  and  a  large  proportion  have  otitis 
media,  latent  or  evident.-^  The  movement  is  more  vigorous  than 
that  of  spasmus  nutans,  it  is  unassociated  with  nystagmus,  and  it 
ceases  when  the  child  sits  up,  only  occurring  when  he  lies  down. 

Rhythmic  tremor  sometimes  occurs  in  gross  brain  disease. 
Thus,  for  example,  in  cases  of  lesions  in  the  tegmental  region 
of  the  pons  or  crus  cerebri,^  affecting  the  ruhro-spinal  tract 
(which  descends  from  the  red  nucleus  into  the  lateral  column  of 
the  opposite  side),  or  in  lesions  of  the  lenticular  nucleus,  we 
occasionally  observe  a  slow  rhythmic  tremor  of  the  limbs  cf 
the  opposite  side,  chiefly  in  the  hand  and  foot.  This  tremor  is 
increased  by  excitement  or  voluntary  movement,  but  ceases  during 
sleep.  In  the  diagnosis  of  such  cases  we  have,  besides  the  tremor, 
the  other  localising  signs  of  a  gross  destructive  lesion.  Thus  if 
the  ocular  nuclei  (which  lie  dorsal  to  the  red  nucleus)  be  affected, 
there  is  ocular  palsy  of  the  nuclear  type ;  if  the  pyramidal  tract 
be  affected  there  is  spastic  hemiplegia ;  and  if  the  sensory  tract, 
traversing  the  internal  capsule  and  optic  thalamus,  be  implicated, 
we  have  hemiansesthesia.  When  a  unilateral  lesion  of  one  crus 
cerebri  produces  oculomotor  paralysis  of  one  side  with  tremor  of 
the  opposite  arm  and  leg,  this  is  known  as  Benedikt's  syndrome. 
Moreover,  certain  lesions  of  the  optic  thalamus  cause  loss  of  emo- 
tional mobihty  in  the  opposite  side  of  the  face,  with  little  or  no 
weakness  on  voluntary  movement. 

In  some  cases  of  tumour  of  the  frontal  lobe,  there  is  a  fine 
tremor  in  the  upper  limb  when  it  is  held  horizontally  forwards. 
The  tremor  in  such  cases  affects  the  ipso-lateral  limb  ;  thus  in  a 
right-sided  frontal  tumour  we  may  find  tremor  in  the  right  hand. 

Let  us  now  pass  to  the  irregular,  non-rh3rthmic,  spontaneous 

'   Still,  Clinical  Journal,  Nov.  28,  1906. 
^  Holmes,  Brain,  1904,  vol.  xxvii.  p.  327. 


INVOLUNTARY    MOVEMENTS  87 

movements.  Of  these,  ordinary  "  rheumatic  "  chorea  furnishes 
one  of  the  most  striking  examples.  All  are  familiar  with  the 
irregular,  jerking,  wriggling,  grimacing  movements  of  a  choreic 
child.  They  may  affect  the  face,  soft  palate,  tongue,  trunk,  limbs, 
and  even  the  muscles  of  respiration.  The  movements  of  the 
limbs  are  often  more  marked  on  one  side  than  on  the  other,  and 
may  be  confined  to  one  side — so-called  hemi-chorea.  Choreic  move- 
ments occur  spontaneously  but  are  increased  by  emotion  or  by 
voluntary  movements.  They  cease  during  sleep.  The  muscles 
of  choreic  limbs  have  a  tonus  which  is  less  than  normal — 
hypotonia.  A  good  method  of  eliciting  choreic  movements  in  a 
slight  case  of  the  disease,  is  to  make  the  child  hold  both  hands 
above  the  head,  when  after  a  few  seconds  slight  involuntary  move- 
ments appear  in  the  fingers  of  one  or  both  sides. 

Huntington's  chorea  is  a  hereditary  variety  of  chorea  which 
comes  on  after  middle  life  and  becomes  steadily  worse.  It  is  asso- 
ciated with  progressive  dementia. 

Hyoscine  chorea,  whose  symptoms  are  similar  to  those  of  ordi- 
nary chorea,  occurs  during  acute  intoxication  with  hyoscine,  and 
is  sometimes,  but  not  invariably,  associated  with  mild  delusions. 

The  movements  of  athetosis  or  "  mobile  spasm  "  are  different, 
occurring  as  they  do  most  commonly  in  the  spastic  limbs  of  old 
hemiplegics  (chiefly  after  infantih  hemiplegia).  Athetosis  never 
occurs  in  a  limb  which  is  completely  paralysed,  but  only  when  some 
degree  of  voluntary  power  survives.  The  movements  are  usually 
confined  to  the  upper  limb,  and  conr^ist  of  very  slow,  irregular,  twist- 
ing movements,  most  marked  in  the  fingers  and  wrist,  but  in  severe 
cases  affecting  the  forearm,  elbow,  shoulder,  and  even  the  lower 
limb,  where  the  most  common  involuntary  movement  is  a  hyper- 
extension  of  the  great  toe.  Only  in  bilateral  athetosis  (generally, 
though  not  always,  following  diplegia)  do  the  movements  affect  the 
face,  causing  hideous  grimacing  (see  Fig.  48,  p.  114).  In  a  typical 
case  the  hand  movements  consist  of  slow  flexion,  then  hyper-exten- 
sion and  spreading  out  of  the  fingers,  irregularly,  one  after  another. 
Combined  with  this  there  is  alternate  abduction  and  opposition  of 
the  thumb,  with  flexion  or  extension  of  the  wrist,  and  pronation  or 


88  NERVOUS    DISEASES 

supination  of  the  forearm.  Figs.  38  to  41  are  taken  from  a  well- 
marked  case  of  athetosis  in  which  the  movements  affected  all  the 
joints  of  the  upper  limb.  Athetosis  is  intensified  by  voluntary 
movement  whether  of  the  paralysed  hmb  or  of  the  opposite 
unaffected  hand.  It  cannot  be  controlled  by  voluntary  effort, 
and  sometimes  persists  even  during  sleep. 


38 


39 


Figs.  38  to  41.— Athetosis  in  a  woman  aged  29,  the  subject  of  right-sided 
hemiplegia  of  nineteen  years  duration.  There  was  severe  paralysis  of  the 
right  upper  limb  from  the  shoulder  downwards.  The  figures  show  athetosis 
of  fingers,  wrist,  and  elbow. 

Spontaneous  "  associated  movements "  occur  involuntarily  in 
many  cases  of  hemiplegia  where  the  paralysis  is  incomplete.  Thus 
the  patient,  when  attempting  to  draw  up  the  hemiplegic  leg,  in- 
voluntarily dorsiflexes  the  ankle  and  hyper-extends  the  hallux,  or 
when  flexing  the  fingers,  he  involuntarily  dorsiflexes  the  wrist,  and 
so  on.     (See  later,  p.  214.) 

Many  healthy  people  make  automatic  extension  movements  of 


INVOLUNTAKY    MOVEMENTS 


89 


the  upper  limbs  during  the  act  of  yawning.  By  the  ancients 
these  were  termed  pandiculation.  Such  movements  are  often 
well  seen  in  the  paralysed  limbs  of  a  case  of  severe  hemiplegia 
when  the  patient  yawns  or  is  tickled,  and  the  patient  may  harbour 
vain  hopes  of  a  return  of  motor  power  by  observing  extension 
movements  of  his  paralysed  fingers  or  elevation  of  the  paralysed 
arm.  Unfortunately  these  movements  are  not  a  hopeful  sign  in 
hemiplegia ;  on  the  contrary,  the  more  severe  the  lesion  of  the 
pyramidal  tract,  the  more 
marked  is  the  pandiculation. 
It  does  not  occur  in  limbs 
which  are  the  subjects  of 
athetosis  or  other  involun- 
tary movements.  Pandicu- 
lation has  been  ascribed  by 
Bertolotti  ^  to  irritation  of 
the  thalamic  centres. 

Spontaneous  movements 
also  occur  in  cases  of  ad- 
vanced Friedreicli's  ataxia, 
being  most  marked  in  the 
head,  neck,  and  face.  They 
commonly  consist  in  irregu- 
lar nodding  movements  of 
the  head  or  grimacing,  which 
has  been  called  "  nystagmus  of  the  face."  But  in  Friedreich's 
ataxia  the  most  outstanding  feature  is  inco-ordination  of  volun- 
tary movements.  The  absence  of  the  knee-jerks,  the  deformity 
of  the  feet,  the  scoUosis,  &c.,  will  all  point  to  a  correct  diagnosis. 

Spontaneous  movements,  pseudo-athetosis,  also  occur  in  certain 
cases  of  tabes  where  tbere  is  severe  impairment  of  joint-sense  and 
ataxia  of  the  muscular  tonus.  The  movements  are  chiefly  seen 
in  the  fingers  and  wrists,  and  can  best  be  demonstrated  by  making 
the  patient  close  his  eyes  and  hold  his  hands  steadily  in  the  air 
with,  the  fingers  extended.     In  a  few  seconds  we  observe  slow 

1  Revue  neurologique,  1905,  p.  953. 


Fig.  42. — Tabetic  pseudo-athetosis  on 
closing  the  eyes. 


90  NERVOUS    DISEASES 

irregular  flexion  or  extension  movements  of  the  fingers,  which 
gradually  assume  curiously  distorted  attitudes,  of  which  the  patient 
is  totally  unaware.  (See  Fig.  42,  also  Fig.  164,  p.  308,  where  similar 
movements  have  occurred  in  the  lower  limbs.) 

Again,  in  general  paralysis  of  the  insane,  spontaneous  tremors 
of  an  irregular  tjrpe  are  frequently  observed,  even  when  the  patient 
is  at  rest.  They  occur  chiefly  in  the  face,  especially  if  the  patient 
be  emotionally  excited  or  just  about  to  speak.  Waves  of  fibrillary 
tremor  appear,  rippling  along  the  muscles  of  the  lips,  tongue,  and 
face.  Irregular  tremors  of  an  intentional  type  are  also  frequently 
present,  especially  in  the  upper  limbs.  Their  rhythm  varies  from 
5  to  9  per  second.  They  can  often  be  demonstrated  by  asking  the 
patient  to  write.  Here  we  have  other  physical  signs  to  guide  us, 
e.g.  the  slurring  articulation,  the  irregular  or  unequal  pupils,  fre- 
quently of  Argyll-Eobertson  type,  exaggeration  or  loss  of  the 
knee-jerks,  the  condition  of  the  cerebro -spinal  fluid,  and  the  char- 
acteristic mental  symptoms. 

There  is  another  great  group  of  involuntary  movements  which 
includes  the  habit  spasms,  the  tics,  and  the  reflex  spasms.  A 
proper  classification  of  these  is  well-nigh  impossible,  since  the 
diflerent  varieties  merge  into  each  other.  All  are  most  common 
in  people  of  "  nervous "  constitution,  all  are  increased  by 
emotion,  and  they  cease  during  sleep.  Slight  degrees  of  habit- 
spasm  may  occur  without  any  other  sign  of  functional  disease. 
Public  speakers,  such  as  clergymen,  barristers,  actors,  and  even 
medical  lecturers,  occasionally  have  little  unconscious  "  tricks " 
of  movement.  A  distinguished  university  professor  has  frequent 
clonic  jerks  of  the  frontales  muscles,  which  suddenly  elevate  his 
eyebrows  ;  a  popular  comedian  makes  rapid  bhnking  movements 
of  both  eyes  (blepharo-spasm)  when  he  advances  towards  the 
foot-lights ;  a  young  lady  has  clonic  spasms  of  both  platysmata 
when  her  neck  is  exposed  in  evening  dress  at  dinner  parties,  and 
so  on.  Such  minor  degrees  of  habit-spasm  are  usually  bilateral 
and  occur  without  any  local  exciting  cause. 

More  severe  varieties  of  habit -spasm  are  included  under  the 
term  "Tic."     A  tic  is  of  cortical,  not  reflex  origin,  and  consists 


INVOLUNTARY   MOVEMENTS 


91 


in  tlie  frequent  explosive  repetition  of^the  same  motor  act — gener- 
ally a  violent,  irregular  one,  such  as  rapid  shaking  or  tossing  of 
the  head,  grimacing,  wriggling  of  the  shoulder,  &c.  It  passes  of! 
as  suddenly  as  it  comes  on.  Moreover,  it  does  not  interfere  with 
voluntary  movements.  For  example,  however  violent  a  tic  of  the 
right  shoulder  or  arm  may  be,  the  patient's  handwriting  shows 
no  abnormality.  As  Patrick  ^  has  put  it,  when  the  impulse  to  tic 
can  no  longer  be  controlled,  the  patient  takes  pen  from  paper, 
executes  his  tic  and  then  resumes 
writing.  At  first  sight,  tic  might 
be  confounded  with  chorea.  But 
chorea  does  not  repeat  the  same 
movement  regularly  again  and 
again.  Patients  who  have  severe 
tic  usually  show  signs  of  mental 
degeneracy.  This  does  not  mean 
that  they  are  necessarily  de- 
ficient in  intelligence.  On  the 
contrary,  they  are  often  "  supe- 
rior degenerates,"  bright  and 
lively,  but  mentally  immature, 
capricious,  emotional,  psychas- 
thenic, and  frequently  the  sub- 
jects of  obsessions  and  various 
forms  of  "  phobia."     The  greater 

the  psychical  abnormality,  the  more  inveterate  is  the  tic. 
"  Tiqueurs  "  often  have  explosive  articulation,  "  word-swallowing," 
sudden  stoppage  of  speech,  disordered  respiration,  echolalia  (repeti- 
tion of  a  particular  word  or  phrase),  or  coprolalia  (repetition  of  a 
blasphemous  or  obscene  word). 

Spasmodic  torticollis  is  one  of  the  commonest  and  most  severe 
varieties  of  tic.  Though  the  movement  of  the  head  is  apparently 
a  unilateral  one,  the  head  being  jerked  constantly  to  one  side, 
commonly  to  the  left  (see  Fig.  43),  it  is  really  a  bilateral  affair, 
since  muscles  on  both  sides  of  the  neck  are  employed  to  produce 


,-M 


Fig.  43. — Spasmodic  torticollis,  with 
secondary  hypertrophy  of  right 
sterno-mastoid. 


1  Journal  of  American  Med.  Assoc,  Feb.  21,  1905 


92  NERVOUS    DISEASES 

the  movement,  and  it  is  sometimes  combined  with,  a  backward 
jerk,  a  so-called  retro-coUic  spasm.  The  movement  may  be  tonic, 
clonic,  or  a  combination  of  the  two — tonico-clonic.  The  patient 
can  often  curb  the  movement  by  means  of  some  antagonistic 
gesture  of  his  own  invention,  e.g.  by  light  pressure  on  the  chin  with 
his  finger.  Severe  torticollis  usually  begins  after  middle  life.  At 
first  occurring  in  paroxysms,  it  ultimately  becomes  continuous 
during  waking  hours,  and  the  affected  muscles  become  hyper- 
trophied  from  over-use. 

Besides  idiopathic  spasmodic  torticollis,  which  comes  on  ap- 
parently spontaneously,  certain  cases  have  a  definite  exciting 
cause  and  should  be  classed,  not  with  the  tics,  but  with  the  reflex 
spasms  which  we  shall  consider  presently.  Thus,  for  example, 
we  may  have  neuralgic  torticollis^  in  which  an  occipital  neuralgia 
or  a  painful. tooth  is  followed  by  spasmodic  torticollis,  usually  tonic 
in  form.  When  the  neuralgia  passes  off,  the  muscular  spasm  ceases 
also.  Again,  we  may  have  labyrinthine  torticollis^  due  to  chronic 
irritation  of  one  of  the  semicircular  canals.  In  such  cases  the 
torticollic  spasm  has  the  object  of  mitigating  vertigo,  which  would 
occur  if  the  head  were  not  kept  leaning  over  to  the  opposite  side. 
A  torticollis  thus  initiated  may  become  inveterate,  but  some  cases 
are  cured  by  the  administration  of  quinine.  A  small  proportion 
of  cases  are  examples  of  professional  torticollis,  occurring  only  at 
the  moment  of  performing  a  special  act,  especially  in  cobblers  and 
tailors,  who  have  to  turn  the  head  and  eyes  to  follow  the  needle. 
Such  cases  are  more  properly  to  be  classed  with  the  occupation- 
neuroses  (see  p.  253).  Spasmus  nutans,  head-rolling,  and  other 
rhythmic  movements  (see  p.  86),  must  not  be  confounded  with 
true  torticollis,  in  which  the  spasms  are  either  tonic  or  irregularly 
clonic. 

There  is  another  group  of  movements  which,  originally  excited 
by  some  peripheral  irritation,  are  classed  as  reflex  spasms.  A 
spasm,  unhke  a  tic,  begins  locally,  perhaps  in  a  single  muscle, 
and  spreads  to   adjacent  muscles.      When  the   exciting  stimulus 

^  Cruchet,  Traite  des  Torticolis  Spasmodiques,  Paris,  1907. 

-  Curschmann,  Deutsche  Zeitschrift  filr  Nervenheilkunde,  1907,  p.  305. 


INVOLUNTARY    MOVEMENTS  93 

is  unilateral,  the  reflex  spasm  is  usually  unilateral  also,  but 
not  invariably  so,  for  bilateral  reflex  spasms  also  occur,  as  in 
tonic  and  clonic  contraction  of  tbe  orbiculares  oculorum  (ble- 
pharospasm), the  result  of  corneal  or  conjunctival  inflammation, 
or  as  in  the  case  where  a  vaginal  caruncle  or  anal  fissure 
produces  vaginismus  with  bilateral  adductor  spasm.  Of  the 
unilateral  reflex  spasms  one  of  the  most  striking  is  the  intense 
facial  spasm  which  occurs  in  severe  cases  of  trigeminal  neuralgia  or 
tic  douloureux,  which  is  not  a  true  tic  but  a  reflex  spasm.  In 
this  disease  the  patient  has  paroxysms  of  agonising  pain  in  one  or 
more  divisions  of  the  trigeminal  nerve.  During  a  paroxysm,  the 
face  on  the  side  of  the  pain  is  thrown  into  strong  tonic  con- 
traction, the  eye  is  closed,  the  mouth  is  drawn  up  on  the  affected 
side,  and  the  patient  often  presses  his  hand  desperately  over 
the  site  of  pain.  Only  when  the  acute  stage  of  the  paroxysm 
passes  of?  do  the  facial  muscles  relax.  Less  severe  facial  hemi- 
sfasm,  either  tonic  or  clonic,  imphcating  some  or  all  of  the  facial 
muscles,  may  arise  from  other  reflex  causes,  generally  in  the 
territory  of  the  fifth  nerve,  such  as  a  decayed  tooth,  a  non-erupted 
wisdom-tooth,  a  nasal  polypus,  &c.  Facial  hemi-spasm,  unlike 
tic  douloureux,  is  painless.  It  also  occurs,  less  frequently,  in 
lesions  of  the  facial  nerve  itself,  as,  for  example,  when  tumours 
or  abscesses  compress  the  nerve.  Sometimes  it  follows  an  attack 
of  ordinary  facial  palsy,  less  commonly  it  may  precede  its  onset, 
so  that  in  every  case  of  facial  hemi-spasm  we  should  search 
for  local  lesions  in  the  territory  not  only  of  the  trigeminal  but 
also  of  the  facial  nerve. 

Sometimes  a  reflex  spasm  may  persist  as  a  habit-spasm,  long 
after  the  original  exciting  cause  has  passed  away.  Such  cases 
can  usually  be  diagnosed  by  their  history.  For  example,  a  lad 
lost  his  left  arm  by  avulsion  in  a  machinery  accident.  The  stump 
was  amputated  at  the  shoulder- joint,  but  clonic  spasms  appeared 
in  the  trapezius  and  scapular  muscles,  and  these  persisted  after 
all  the  posterior  nerve-roots  in  that  region  were  divided  by 
operation.  But  other  cases  occur,  even  of  unilateral  spasm,  with- 
out  any  reflex  exciting   cause   or  the  history  of  one,  and  they 


94  NERVOUS    DISEASES 

are  difficult  to  classify.  Thus  a  lady  whose  menopause  oc- 
curred at  the  age  of  forty-five,  at  the  same  time  also  lost  most 
of  her  property  through  the  failure  of  a  bank.  She  gradually 
developed  clonic  spasm  of  the  left  facial  muscles.  At  first,  this 
consisted  merely  in  a  slight  flickering  of  the  lower  lid  for  a  second 
or  two,  every  few  days,  but  the  condition  gradually  increased  in 
severity  until,  when  she  came  under  observation  thirteen  years 
later,  the  spasms  affected  all  the  facial  muscles  on  one  side,  be- 
ginning as  a  flickering  movement,  and  then  becoming  tonic  and 
lasting  from  twenty  to  thirty  seconds  at  a  time,  the  eye  being 
closed,  the  eyebrow  elevated,  the  angle  of  the  mouth  drawn  out- 
wards, and  the  platysma  thrown  into  strong  contraction.  In  the 
intervals  between  attacks  the  face  was  symmetrical.  Under  treat- 
ment by  bromides  and  galvanism  this  case  became  rapidly  better. 
Finally,  there  are  numberless  varieties  of  hysterical  spasms, 
apart  from  the  hysterical  "  fits,"  which  have  already  been  dis- 
cussed. We  can  only  refer  to  some  of  the  commoner  types. 
Thus  saltatory  spasm  consists  of  a  series  of  jumping  or  skipping 
movements,  which  occur  whenever  the  patient  assumes  the  erect 
posture.  A  similar  spasm,  less  severe  in  degree,  may  produce 
paroxysms  of  trembling  in  the  legs,  as  in  a  hysterical  girl  of  nineteen 
with  many  other  stigmata  of  hysteria,  in  whom  the  spasms  ceased 
at  once  when  she  lay  down.  All  sorts  of  movement,  however, 
may  occur  in  hysteria,  simulating  almost  any  kind  of  tremor. 
For  instance,  a  hysterical  woman  of  twenty-one  had  constant 
movements  of  the  face,  left  arm,  and  both  legs,  resembling  those  of 
athetosis  but  very  much  faster.  In  her  case  t3^pical  hysterical 
contractures  and  segmental  anaesthesia  of  the  hysterical  type, 
together  with  the  normal  state  of  the  reflexes,  aided  in  the 
diagnosis  of  hysteria,  which  disease  will  be  further  considered  in  a 
subsequent  chapter. 


CHA.PTER   VII 

APHASIA 

We  exchange  ideas  with  our  fellow-men  chiefly  by  means  of  speech. 
Speech  is  an  arbitrary  code  of  signals,  vocal  or  written.  These 
signals  are  perceived  by  om-  auditory  or  visual  centres.  Every 
country  has  its  own  particular  code  or  language,  which  is  learned 
by  each  of  its  inhabitants.  Gestures  and  mimic  movements,  as 
a  means  of  communication,  although  international,  have  a  very 
limited  field  of  usefulness  as  compared  with  speech.  Two  indi- 
viduals, each  ignorant  of  the  other's  language,  can  certainly  com- 
municate with  each  other  after  a  fashion  by  means  of  gestures 
alone,  yet  they  cannot  express  many  ideas  in  this  way,  but 
only  simple  primitive  emotions  such  as  pleasure,  anger,  surprise, 
and  so  on,  or  pantomimic  imitations  of  certain  acts. 

There  are  three  chief  classes  of  cases  in  which  the  functions 
of  articulate  speech  may  be  lost.  Firstly,  there  are  conditions  in 
which  the  patient's  higher  intellectual  functions  are  in  abeyance, 
either  congenitally  as  in  idiots,  or  from  disease  as  in  acquired 
dementia,  coma,  stupor,  or  in  certain  cases  of  hysteria.  Such 
patients  are  speechless,  but  they  are  not  aphasics.  Secondly,  there 
are  the  cases  where  the  higher  intellectual  centres  are  capable 
of  function,  but  the  cortical  speech-centres  which  control  the 
motor  acts  of  speaking  and  writing,  or  the  sensory  processes  of 
recognising  spoken  or  written  words,  are  diseased,  and  yet  the 
patient  has  not  necessarily  any  paralysis  of  the  peripheral  organs  of 
speech,  nor  is  he  necessarily  deaf  or  blind.  To  this  group  the  term 
"  aphasia  "  is,  applied.  Lastly,  there  are  the  cases  where,  with 
intact  intellectual  functions  and  normal  cortical  speech-centres, 
there  are  defects  in  the  peripheral  organs  of  articulation,  £.0  that 
th3   patient  is  unable  to  aiticulate  distinctly — for  example,  cases 

of  cleft  palate,  post-diphtheritic  palsy  of  the  palate,  facial  or  hypo- 

95 


96 


NERVOUS    DISEASES 


glossal  paralysis,  bulbar  paralysis,  and  so  on.     These  are  affections, 
not  of  speecb  proper,  but  of  articulation. 

Aphasia  may  be  defined  as  impairment  or  loss  of  speech,  due 
to  the  loss  of  memory  for  those  signs,  vocal  or  written,  by  means 
of  which  we  exchange  ideas  with  our  fellow-men.  An  aphasic, 
unless  his  higher  intellectual  centres  are  impaired,  usually  pre- 
serves his  powers  of  gesture  and  of  pantomime.  Aphasia  is  due 
to  disease,  organic  or  functional,  of  certain  well-defined  special 
centres  in  or  near  the  cortex  of  the  brain.     These  cortical  centres 


Fig.  44. — Diagram  of  left  cerebral  hemisphere,  showing  approximate 
positions  of  the  centres  concerned  in  speech. 

A.  Auditory  word-centre.        \v.pu^nrv 

V.  Visual  word-centre.  |  sensory. 

Sp.  Vocal  word-centre.  \  -\r„t„_ 

W.  Motor  centre  for  writing,  j^''^"'-"'- 

exist  on  both  sides  of  the  brain,  but  ordinarily  in  right-handed 
people  the  speech-centres  on  the  left  side  of  the  brain  are  pre- 
dominant. 

Let  us  consider  the  speech-centres  somewhat  more  in  detail. 
For  the  interchange  of  ideas  two  distinct  processes  are  required — 
one  sensory,  the  other  motor.  The  sensory  process  includes  the 
hearing  and  understanding  of  spoken  words,  and  also  the  seeing  and 
understanding  of  written  or  printed  letters.  The  memories  of 
words  heard  and  seen  are  stored  up  in  specialised  parts  of  the 
auditory  and  visual  centres,  named  respectively  the  auditory  word- 
centre  and  the  visual  word-centre  (Fig.  44).  The  auditory  word- 
centre  is  at  the  upper  or  Sylvian  surface  of  the  temporal  lobe 
(anterior  transverse  gyrus  of  Heschl,  Flechsig's  "  auditory  gyrus  ") 


APHASIA  97 

and  in  the  adjacent  posterior  end  of  the  first  temporal  convolution  ; 
the  visual  word-centre  is  in  the  angular  gyrus.  Either  centre  may 
be  diseased  ;  so  that  we  have  two  varieties  of  sensory  aphasia, 
viz. — auditory  aphasia  and  visual  aphasia.  Then  there  is  in 
speech  the  motor  element,  consis1?ing  of  the  motor  act  of  expressing 
ourselves  in  words,  either  vocally  or  by  means  of  writing.  The 
memories  of  these  motor  acts  of  vocal  speech  are  ordinarily  sup- 
posed to  be  stored  up  at  the  posterior  end  of  the  inferior  frontal 
(Broca's)  convolution,  and  in  the  adjacent  part  of  the  pre-central 
convolution  and  of  the  insula.  If  this  centre  be  destroyed,  motor 
aphasia  or  aphemia  is  said  to  result,  the  patient  being  unable  to  utter 
words  of  which  his  motor  memories  have  been  destroyed.  Marie, 
however,  has  recorded  cases  of  destruction  of  Broca's  convolution 
without  any  speech  defect,  and  denies  that  it  has  any  special  im- 
portance in  the  mechanism  of  speech.  He  considers  that  cases  of  so- 
called  motor  aphasia  are  really  examples  of  ordinary  sensory  aphasia 
combined  with  articulative  difficulty  (anarthria  or  dysarthria)  due 
to  a  lesion  of  the  lenticular  nucleus  and  its  surrounding  white  matter, 
and  maintains  that  isolated  lesions  of  Broca's  convolution  are 
accidental  and  of  minor  significance.  Earlier  writers  used  also  to 
describe  a  separate  centre  for  writing  (independent  of  the  vocal 
word-centre),  a  lesion  of  which  would  produce  loss  of  the  faculty 
of  writing — agraphia.  But  no  case  has  been  verified  pathologically 
in  which  a  focal  lesion  has  produced  pure  agraphia  without  affec- 
tion of  vocal  speech,  so  that  the  writing-centre,  although  it  may 
be  represented  diagrammatically  in  a  theoretical  scheme  of  cortical 
speech-centres,  is  probably  merely  a  part  of  the  ordinary  psycho- 
motor centre  for  the  upper  extremity. 

Fig.  45  is  a  scheme  of  the  connection  of  the  various  centres 
concerned  in  speech.  Let  us  first  notice  that  the  motor  vocal 
word-centre  is  subservient  to  the  auditory  word-centre,  and  that 
the  writing-centre  is  similarly  subservient  to  the  visual  word- 
centre.  A  child  learns  to  speak  first  by  hearing  spoken  words 
and  then  imitating  them.  Therefore  speech  at  first  is  entirely 
auditory  in  origin.  Later,  in  learning  to  read,  the  meaning  of  each 
word  is  learned  by  associating  the  letters  seen  with  words  heard 


98 


NERVOUS   DISEASES 


spoken,  so  that  the  auditory  word-centre  acts  as  the  instructor  of 
the  visual  word-centre. 

In  most  people,  during  the  process  of  silent  thought,  words 
are  revived  primarily  in  the  auditory  word-centre,  and  there  is 
usually  a  simultaneous  revival  of  the  same  words  in  the  visual 
word-centre.  But  in  other  people  the  revival  in  the  visual  word- 
centre  comes  to  be  of  greater  importance.  Accordingly  we  may 
classi  y  people  into  "  auditives  "  and  "  visuals  "  according  to  their 
mode  of  revival  of  words  in  thought.     Most  of  us  are  "  auditives." 


Fig.  45. — Diagram  of  Speech-Centres  (after  Bramwell). 

A.  Auditory  word-centre.  V.  Visual  word-centre. 

Sp.  Motor  vocal  word-centre.        W.  Motor  centre  for  writing. 
HV.  Half-vision  centre. 

Tiie  interrupted  lines  indicate  possible  but  less  habitual  routes  for  transmission  of  impulses. 

Simultaneous  revival  of  word-images  in  several  speech-centres 
makes  our  comprehension  of  the  idea  more  perfect.  Thus  a 
difficult  concept  is  better  understood  if  we  read  it  aloud,  because 
this  involves  the  activity  of  the  visual,  auditory  and  vocal 
word-centres. 

Aphasia  commonly  results  from  organic  disease  of  one  or  more 
of  the  cortical  speech-centres,  or  of  the  sub-cortical  fibres  connect- 
ing them.  The  most  frequent  organic  causes  are  embolism,  haemor- 
rhage, or  thrombosis,  cerebral  abscesses  and  cerebral  tumours.  The 
differential  diagnosis  between  these  various  conditions  depends 
largely  on  the  history ;  embolism  producing  the  symptoms  suddenly, 
hflemorrhage  taking  several  minutes,  thrombosis  taking  perhaps 
hours,  abscess  and  tumours  being  still  more  gradual  in  onset.     But 


APHASIA  _  99 

we  also  meet  with  cases  of  temporary  or  functional  aphasia, 
sometimes  from  mere  debility  or  exhaustion,  sometimes  from 
locahsed  vascular  spasm,  sometimes  following  a  "congestive 
attack "  in  general  paralysis,  or  accompanying  a  paroxysm  of 
migraine,  or  an  attack  of  uraemia,  or  after  an  epileptic  fit. 

In  investigating  a  case  of  aphasia  we  should  first  note  whether 
the  patient  has  other  signs  of  gross  cerebral  lesion,  such  as 
hemianopia,  or  hemiplegia,  and  should  inquire  whether  he  is 
naturally  right-  or  left-handed.  Most  children  are  taught  to  write 
with  the  right  hand,  whether  they  are  right-handed  or  not,  and 
therefore  in  determining  this  point  we  inquire  with  which  hand 
a  man  draws  a  cork,  throws  a  stone,  &c.  ;  or  if  a  woman,  with 
which  hand  she  combs  her  hair  or  threads  a  needle  ;  or,  in  either 
sex,  which  hand  is  used  in  cutting  bread. 

The  following  series  of  inquiries  (based  on  Besvor's  scheme) 
should  then  be  made.  The  capital  letters  in  parenthesis  indicate 
the  parts  of  the  brain  involved  in  each  case. 

1.  Can  the  patient  spontaneously  utter  intelhgible  words  ? 
(Sp.)  Note  the  extent  of  his  vocabulary.  Can  he  pronounce  all 
words  or  only  a  few  ?  Get  the  patient  to  talk  spontaneously,  and 
observe  whether  he  talks  fluently  or  misplaces  words  or  syllables, 
whether  he  talks  in  disjointed  phrases,  ("  telegraphic  "  type  of 
speech,)  or  whether  he  talks  unintelligible  jargon. 

2.  Can  he  understand  words  which  he  hears  ?  (A.)  Ask  him 
to  touch  his  nose,  ear,  eye,  chin,  &c.,  in  turn,  thus  testing  his 
interpretation  of  nouns.  Then  ask  him  to  smile,  whistle,  shut 
his  eyes,  &c.,  thus  testing  his  comprehension  of  verbs.  Some- 
times we  find  that  the  patient  executes  the  first  coramand  correctly, 
but  continues  to  repeat  the  same  act  in  response  to  different 
commands.  A  patient  can  sometimes  sing  the  words  and  air  of 
a  song,  when  he  is  unable  to  repeat  the  words  in  a  speaking 
voice. 

3.  Can  he  understand  written  questions  or  commands  which 
he  sees  ?  (V.)  Write  doAvn  and  show  him  simple  sentences,  such 
as  "  How  old  are  you  ?  "  "  Put  out  your  tongue."  "  Give  me 
your  left  hand." 

4.  Can  he    write  spontaneously  ?     (W-)     If  his  right  hand  is 


100  NERVOUS    DISEASES 

paralysed,  let  him  try  with  the  left.  Observe  whether  he  writes 
intelHgibly,  whether  he  misplaces  words  or  syllables,  or  whether  he 
scribbles  meaningless  signs. 

5.  Can  he  copy  from  printed  to  written  letters  ?  (V^W.) 
Print  some  word  such  as  "  Hospital  "  or  "  Monday,"  and  get  him 
to  copy  this. 

6 .  Can  he  write  to  dictation  words  which  he  hears  ?    ( A  -^  V  ->  W. ) 

7.  Can  he  pick  out  objects  of  which  he  hears  the  name  ? 
(A^V-)  Place  in  front  of  him  a  heap  of  objects,  such  as  a  key, 
a  shilling,  a  match,  a  pencil,  and  ask  him  to  pick  out  each  in  turn. 

8.  Can  he  repeat  words  heard  ?  (A-'Sp.)  Try  him  first  with 
simple  words  and  phrases  ;  e.g.  "  cat,"  "  dog,  '  "  nurse,"  "  good- 
morning,"  &c. 

9.  Can  he  name  objects  seen,  and  can  he  read  aloud  from  words 
shown  to  him?  (V^A^Sp-)  Point  to  different  objects  and  ask 
him  what  they  are. 

10.  Does  he  understand  gestures  and  pantomimic  movements  ? 
Without  speaking  to  him,  get  him  to  imitate  you  when  touching 
the  nose,  spreading  out  the  fingers,  protruding  the  tongue,  &c. 

Auditory  Aphasia,  or  Word-Deafness. — The  patient  in  this 
case  is  not  deaf,  but  simply  word-deaf.  He  hears  ordinary  sounds 
and  noises,  but  spoken  words  are  not  understood ;  they  sound  to 
him  like  an  unknown  tongue.  The  character  of  the  symptoms 
varies  according  as  the  lesion  is  subcortical  or  cortical  in  position. 

{a)  Subcortical,  or  Pure  Auditory  Aphasia. — This  is 
extremely  rare  (Marie,  in  fact,  denies  its  existence).  Here  the 
lesion  simply  blocks  the  way- in  for  spoken  words.  The  patient 
therefore  has  word-deafness — i.e.  he  is  unable  to  understand  what 
is  said  to  him  ;  he  is  also  unable  to  repeat  spoken  words  or  to  write 
from  dictation.  But  the  auditory  word-centrs  being  still  intact,  he 
possesses  all  his  memories  of  auditory  speech,  and  therefore 
spontaneous  speech  is  perfect.  Moreover,  the  visual  word-centre 
being  in  normal  working  order,  he  is  still  able  to  read,  and,  as 
a  matter  of  fact,  reading  is  his  only  means  of  receiving  messages 
from  other  people. 


APHASIA  101 

(h)  Cortical  Word-Deafness. — This  is  much  commoner  than 
the  other  variety.  Here  the  lesion  involves  the  cortical  centre  itself, 
and  the  auditory  memories  of  spoken  words  are  obliterated.  And 
therefore,  in  addition  to  the  previous  defects  of  wo:d-deafness  with 
inability  to  r  peat  spoken  words  or  to  wiite  from  dictation,  there 
are  other  symptoms  due  to  the  fact  that  the  motor  speech-centre  is 
no  longer  controlled  by  the  auditory  word-centre.  Internal  speech 
and  thought  are  impaired,  and  so  the  patient  makes  mistakes 
whether  in  speaking  spontaneously  or  in  reading  aloud  He  also 
makes  mistakes  in  writing,  especially  in  spelling.  He  talks  fluently 
enough,  it  is  true,  but  he  tends  to  mix  up  his  words  or  syllables, 
and  in  a  severe  case  may  jabber  unintelligible  jargon.  Word- 
deafness  renders  the  patient  unaware  of  his  own  errors.  This,  as 
we  shall  see,  is  in  marked  contrast  with  motor  aphasia,  where  the 
patient  recognises  his  own  mistakes  as  soon  as  he  has  uttered 
them.  If  the  lesion  of  the  auditory  word-centre  be  incomplete, 
the  word-deafness  and  resulting  errors  of  speech  are  also  partial. 
These  latter  may,  in  a  slight  case,  be  confined  to  inability  to  name 
objects,  i.e.  nouns,  the  patient  being  still  able  to  express  abstract 
ideas.  Thus  a  partially  word-deaf  patient,  who  is  unable  to  name 
a  knife  shown  him,  may  say,  "  It  is  for  cultng."  Or  again,  partial 
word-deafness  may  produce  simply  confusion  of  words  ;  the  patient 
may  say  one  word  when  he  means  another  (para'phasia).  It  rarely 
happens  that  word-deafness  remains  permanent  and  complete  ;  the 
auditory  word-centre  in  the  opposite  hemisphere  generally  com- 
pensates, to  some  extent,  as  time  goes  on. 

The  extent  of  mental  disturbance  in  word-deafness  varies  accord- 
ing to  whether  the  patient  be  a  strong  "  auditive  "  or  a  strong 
"visual."  In  the  latter  case  the  mental  impairment  is  much  less  than 
in  the  former,  and  the  disturbances  of  motor  speech  are  but  slight. 

The  auditory  and  visual  word-centres  are  fairly  close  together, 
and  more  than  this,  they  are  supplied  by  the  same  branch  of  the 
middle  cerebral  artery  (see  Fig.  26,  p.  42)  ;  so  that  it  is  not  un- 
common for  a  single  arterial  lesion,  e.g.  a  thrombosis,  to  affect  both 
centres  together  and  to  produce  a  combination  of  word-deafness 
and  word-blindness. 


102 


NERVOUS    DISEASES 


Visual  Aphasia,  or  Word-Blindness  (Alexia). — In  word-blind- 
ness the  patient  can  see,  but  cannot  understand  printed  or  written 
characters.  They  appear  to  bim  Hke  strange  bieroglypbics.  He  sees 
the  shape  of  the  letters,  but  they  convey  no  meaning  to  his  mind. 

Here,  as  in  word-deafness,  the  symptoms  vary  in  degree.  The 
patient  may  be  unable  to  recognise  a  single  letter  (letter-bhndness), 
or  he  may  be  able  to  spell  out  the  letters  singly  but  unable  to  read 
syllables  or  words.  Often  a  patient  who  is  unable  to  read  any 
other  word,  can  recognise  his  own  name.     Frequently  he  retains 

c.c. 


Fig.  46. — Diagram  represeutiDg  a  lesion  ( indicated  by  thick  black  line) 
which  produces  pure  word-blindness  (Bastian). 

C.  C.  Posterior  extremity  of  corpus  callosuni. 

c.  c.     Commissural  fibres  connecting  tlie  two  visual  word-centres. 

6.  b.     Fibres  connecting  each  half-vision  centre  with  the  visual  word-centre  of  the  same  side. 

the  power  of  recognising  numbers  and  of  doing  addition,  sub- 
traction, and  multiphcation  sums.  We  have  to  recognise  two 
varieties  of  word-bhndness,  according  as  the  lesion  is  cortical  or 
subcortical  in  position. 

{a)  Subcortical,  or  Pure  Word-Blindness. — Here  the  way- 
in  for  visual  word-impression  is  destroyed,  the  visual  word- 
centre  remaining  intact.  The  patient  cannot  understand  written 
or  printed  words,  nor  can  he  read  aloud,  but  he  still  retains 
the  power  of  writing  spontaneously  and  from  dictation ;  and 
therefore  he  can  express  his  thoughts  perfectly  in  writing,  but 
is  unable  to  read  what  he  has  himself  written.  Inasmuch  as 
a  subcortical  lesion,  in  order  to  produce  word-bhndness,  must  be 
beneath  the  angular  gyrus  and  in  such  a  position  as  to  cut  off  the 
afierent  visual  impulses  from  both  half -vision  centres  to  the  visual 


APHASIA  103 

word-centre  in  the  angular  gyrus,  it  will  necessarily  implicate  the 
optic  radiation  to  some  extent.  And  therefore  a  pure  or  subcortical 
word-bhndness  is  always  associated  with  hemianopia  or,  when 
paitial,  with  hemi-achromatopsia  (Fig.  46). 

{h)  Cortical  Word- Blindness. — In  this  variety,  in  addition  to 
the  symptoms  just  described,  there  is  loss  of  the  memories  of  written 
or  printed  words,  and  therefore,  inasmuch  as  the  visual  word-centre, 
which  controls  the  writing-centre,  is  destroyed,  the  patient  has 
agraphia.  He  is  unable  to  write  spontaneously,  to  copy  from  printed 
into  written  characters,  or  to  write  from  dictation.  If  the  lesion 
of  the  visual  word-centre  be  partial  the  alexia  and  agraphia  are 
also  incomplete,  and  mistakes  in  writing  may  amount  simply  to 
the  writing  of  wrong  words,  syllables  or  letters — so-called  "  par- 
agraphia.^'' 

These  points  are  illustrated  by  Bramwell's  well-known  diagram 
(Fig.  45),  in  which  a  lesion  at  the  position  marked  1,  destroying 
fibres  passing  from  one  half-vision  centre  to  the  visual  speech- 
centre,  would  not  produce  word-blindness.  A  lesion  at  1,  destroy- 
ing fibres  passing  from  both  half -vision  centres  to  the  visual  speech- 
centre,  would  produce  word-blindness  but  not  agraphia,  since  the 
visual  speech-centre  is  unaffected  and  is  able  to  influence  the 
motor  writing-centre.  A  lesion  at  2,  destroying  the  visual  speech- 
centre,  would  produce  word-blindness  and  agraphia.  A  lesion  at 
3  would  produce  agraphia  (unless  the  motor  writing-centre  could 
be  brought  into  action  in  some  roundabout  way),  but  not  word- 
blindness,  the  visual  speech-centre  being  intact. 

Motor  Aphasia. — In  this  variety  the  patient  has  lost  the 
power  of  expressing  himself  by  spoken  words.  He  can  neither 
speak  spontaneously  nor  can  he  read  aloud.  And  yet  (unless  the 
motor  speech-centres  on  both  sides  of  the  brain  are  destroyed)  he 
is  not  absolutely  dumb.  As  Hughhngs  Jackson  puts  it,  the  patient 
is  speechless,  but  as  a  rule  not  wordless.  He  can  usually  utter 
intelhgently  a  few  words,  such  as  "  yes  "  and  "  no,"  by  means  of 
the  speech-centre  on  the  uninjured  side,  and  in  addition  he  may 
have  other  words  or  phrases,  mostly  interjections,  such  as 
"  oh    my  !  "    "  come    on  !  "     "  damn  !  "    "  by   Jove  !  " — so-called 


104  NEEVOUS    DISEASES 

"  recurrent  utterances " — wliicli  he  utters  automatically  when 
excited,  or  when  making  an  effort  to  speak.  A  patient  who 
has  motor  aphasia,  unlike  a  word-deaf  person,  is  conscious  of  his 
own  errors. 

(a)  Subcortical,  or  Pure  Motor  Aphasia. — Here  the  patient, 
though  intelligent  and  able  to  understand  spoken  and  written 
language  (by  means  of  his  uninjured  auditory  and  visual  word- 
centres),  cannot  utter  spoken  language,  either  spontaneously  by 
reading  aloud  or  by  repeating  what  he  hears.  This  is  because 
the  way-out  for  spoken  speech  is  blocked.  But  his  mental  speech- 
processes  are  unimpaired,  and  if  the  outgoing  fibres  from  the 
writing  centre  are  unimpaired,  he  is  able  to  express  himself  in 
writing,  as  in  the  scriptural  case  of  Zacharias,  the  father  of  John 
the  Baptist  (St.  Luke,  i.  62,  63),  and  in  many  cases  the  patient 
can  indicate  by  signs  how  many  syllables  or  letters  are  in  the 
word  which  he  desires  to  speak  but  cannot  utter.  This  variety  of 
aphasia  sometimes  occurs  in  hysteria.  The  hysterical  aphasic 
cannot  utter  any  sound  whatever,  whether  articulate  or  not. 
Zacharias  was  probably  a  hysterical  aphasic.^ 

(&)  Cortical  Motor  Aphasia. — This  type,  in  which  the  lesion  is 
supposed  to  be  limited  to  the  cortical  motor  speech-centre  in  the 
inferior  frontal  gyrus  and  adjacent  grey  matter  of  the  insula  and 
pre-central  gyrus,  is  less  securely  established  than  the  other  varieties. 
(Marie  denies  its  existence  altogether.)  The  patient  in  this  variety 
has  not  only  all  the  defects  of  a  subcortical  case,  which  we  have 
just  considered,  but,  in  addition,  his  mental  processes  of  internal 
thought  are  impaired,  since  the  co-ordination  of  memories  of  words 
spoken  and  written  by  himself  is  impaired.  He  has  therefore 
difficulty  in  understanding  complicated  sentences,  whether  spoken 
or  written.  Together  with  difficulty  in  vocal  speech  there  is  often 
(though  not  always)  associated  a  similar  difficulty  in  writing — • 
agraphia — proportional  to  the  defect  of  speech. 

Pure  isolated  agraphia,  without  any  other  symptom,  does  not 
occur,  and  as  we  have  seen,  the  commonest  variety  of  agraphia 

1  "  And  liis  mouth  was  opened  immediately,  and  his  tongue  loosed,  and  he 
spake,  and  praised  God." 


APHASIA  105 

is  tliat  due  to  cortical  word-blindness.  The  study  of  agraphia  due 
to  sensory  aphasia  is  easier  than  that  associated  with  motor  aphasia, 
because  in  sensory  aphasia  there  is  no  necessary  motor  paralysis 
of  the  right  arm  or  hand,  whereas  sometimes  in  motor  aphasia  the 
patient  has  to  make  his  attempts  at  writing  with  the  left  hand. 

Such  are  the  chief  types  of  aphasia.  Clinically,  however,  it  is 
commoner  to  meet,  not  with  pure  auditory,  visual,  or  motor 
aphasia,  due  to  a  small  focal  lesion,  but  with  combinations  of 
these,  or  with  total  aphasia,  the  result  of  a  larger  destructive 
lesion  implicating  several  or  all  of  the  speech-centres.  Such  severe 
aphasias,  of  course,  produce  a  more  profound  degree  of  mental 
deficiency,  and  inasmuch  as  the  same  artery,  the  middle  cerebral, 
supplies  not  only  the  speech-centres,  but  also  the  other  cortical 
motor  areas  and  the  corpus  striatum  (see  Figs.  26  and  27),  total 
aphasia  is  usually  combined  with  severe  right  hemiplegia. 

Hysterical  aphasia  is  usually  accompanied  by  other  stigmata  of 
hysteria,  and  especially  by  hysterical  hemiplegia.  It  is  paradoxical 
and  polymorphic,  and  usually  differs  from  organic  aphasia  in  some 
curious  fashion,  according  to  the  caprice  of  the  patient.  Thus, 
for  example,  a  patient  with  hysterical  aphasia  may  also  have 
peculiar  tricks  of  intonation  or  of  accent. 

Marie,!  whilst  admitting  the  existence  of  visual,  auditory  and  motor 
aphcisia  as  clinical  syndromes,  denies  the  existence  of  diagrammatic  visual, 
auditory  and  motor  speech-centres,  and  attributes  all  aphasic  phenomena  to 
intellectual  deficiency  from  disintegration  of  some  part  of  Wernicke's  zone 
(which  consists  of  the  gyri  surrounding  the  extremities  of  the  Sylvian  and 
the  parallel  fissure),  which  zone  he  regards  as  an  intellectual  area.  According 
to  Marie  the  essential  fact  of  aphasia,  of  whatever  variety,  is  insufficient  com- 
prehension of  speech.  He  adduces  evidence  to  show  that  Broca's  convolution 
plays  no  special  part  in  the  function  of  speech  except  in  so  far  as  it  contains 
certain  motor  centres  for  the  face,  tongue  and  larynx.  In  fact  he  discards  a 
special  vocal-word-centre  just  as  others  discard  a  motor  centre  for  writing. 
The  syndrome  of  motor  aphasia  is  explained  by  him  as  due  to  intellectual 
deficiency  ^Zi(s  articulative  anarthria,  this  latter  being  due  to  a  lesion  of  the 
lenticular  zone  (comprising  the  lenticular  nucleus  and  its  surrounding  white 
matter).  In  other  words,  he  regards  motor  aphasia  simply  as  a  sensory 
aphasia  minus  the  power  of  speech.  The  intellectual  processes  of  speech  in 
right-handed  patients  are  localised  in  the  left  hemisphere,  whereas  anarthria 
may  be  produced  by  a  lesion  of  either  lenticular  zone. 

1  Semaine  Medicale,  1906,  Nos.  21,  42,  and  48. 


106  NERVOUS    DISEASES 

But  though  Marie's  views  are  seductive  in  their  simplicity,  there  are 
certain  obstacles  to  accepting  them  in  their  entirety.  Even  supposing  that 
the  only  real  varieties  of  aphasia  are  sensory,  and  that  some  defect  of  intelli- 
gence is  present  iu  every  case,  it  seems  none  the  less  probable  that  visual  and 
auditory  speech-centres  do  exist,  and  that  lesions  of  these  centres,  rather  than 
mere  intellectual  deficiency,  are  the  cause  of  the  well-defined  clinical  types  of 
sensory  aphasia.  As  Dejerine  has  urged,  we  may  have  advanced  dementia 
from  undoubted  cortical  disease,  as  in  general  paralysis,  without  any  aphasia, 
sensory  or  motor.  It  therefore  seems  probable  that  the  diminution  of 
intelligence  which  is  seen  in  aphasic  patients  is  due  to  interference  with 
cortical  sensorial  processes,  producing  disruption  of  the  cerebral  mechanism  of 
speech,  rather  than  that  the  aj)hasic  phenomena  should  be  regarded  as  secondary 
to  intellectual  deficit.  With  regard  to  Marie's  conception  of  motor  aphasia 
as  a  mere  combination  of  intellectual  deficiency  with  anarthria,  it  may  be 
objected  that  this  fails  to  account  for  the  presence  of  well-articulated  "  re- 
current utterances"  such  as  are  present  in  most  patients  with  complete  motor 
aphasia.  If  anarthria  alone  were  the  cause  of  the  speech-loss,  it  ought  to 
render  the  articulation  of  all  words  difficult.  Moreover,  the  cortical  vocal- 
word-centre  is  not  limited  to  Broca's  convolution,  but  probably  extends  into 
the  insula  and  to  the  neighbouring  part  of  the  pre-central  gyrus.  So  that 
there  is  no  insuperable  difficulty  in  the  existence  of  a  lesion  limited  to  Broca's 
convolution  unaccompanied  by  aphasia. 

Apraxia  is  the  inability  to  execute  certain  familiar  purposive 
movements  with,  the  hmbs,  when  there  is  neither  motor  paralysis, 
sensory  disturbance,  nor  ataxia  of  the  Hmb,  nor  any  intellectual 
impairment.  Apraxia  of  the  muscles  of  the  hmbs  is  therefore  ana- 
logous to  motor  aphasia  of  the  speech  muscles.  Certain  functions, 
comparable  to  the  functions  of  speech,  have  their  cortical  centres 
situated  in  the  first  and  second  frontal  gyri  of  the  left  hemisphere, 
these  centres  being  connected  with  the  corresponding  centres  in 
the  right  hemisphere  by  means  of  the  anterior  fibres  of  the  corpus 
c  alio  sum. 

Apraxia  may  be  either  sensory  or  motor  in  type.  Thus  if  an 
apraxic  patient  be  handed  a  tooth-brush  and  asked  to  use  it,  he 
may  put  it  in  his  mouth  and  try  to  smoke  it  like  a  cigar.  Such 
apraxia  is  sensory  in  origin,  due  to  failure  of  recognition.  On  the 
other  hand,  suppose  he  recognises  it  as  a  tooth-brush  and  may 
even  name  it  and  tell  what  it  is  for,  but  when  asked  to  use  it  he 
fumbles  aimlessly  with  it,  his  apraxia  is  motor  in  type.  To  take 
another  example,  motor  apraxia  of  the  tongue  is  often  seen  in  a 
hemiplegic  patient  who  fails  to  protrude  his  tongue  when  told  to  do 


APHASIA 


107 


so,  but  can  still  lick  his  lips  unconsciously.  Sometimes  the  apraxic 
patient  cannot  perform  a  given  series  of  purposive  movements 
unless  he  has  the  sensory  stimulus  of  the  object  in  his  hand,  with 
which  the  movements  are  associated.  For  example,  an  apraxic 
cornet-player  could  not  purse  up  his  lips  to  blow  the  instrument 
miless  he  had  the  actual  mouthpiece  at  his  hps. 

Over  95  per  cent,  of  people  are  right-handed.     In  them  the 
left  cerebral  hemisphere  is  the  dominant  one  and,  besides  controlhng 


X y 

Fig.  17. — Diagram  illustrating  relation  of  corpus  callosum  to  apraxia. 


the  hmbs  of  the  right  side  of  the  bcdy,  it  exercises  a  potent  influence 
upon  the  right  cerebral  hemisphere  by  means  of  the  commissural 
fibres  of  the  corpus  callosum.  Thus  many  movements  of  the  left 
limbs  are  mitiated  by  the  left^  hemisphere,  so  that  a  left-sided 
cortical  or  subcortical  lesion,  if  impHcatmg  the  corpus  callosimi, 
may  produce  not  only  right -sided  hemiplegia  or  monoplegia,  but 
also  apraxia  of  the  non-paralysed  left  hand.  Such  apraxia  of  the 
ipso -lateral  hand  is  evidence  of  a  lesion  of  the  fibres  of  the  corpus 
callosum.  Apraxia  is  associated  with  lesions  of  the  left  hemisphere 
much  oftener  than  with  right-sided  lesions. 


108  NEKVOUS  DISEASES 

Fig.  47  is  a  diagrammatic  representation  of  the  above-mentioned 
points,  which  shows  that : — 

1.  A  lesion  at  or  close  beneath  the  left  arm- centre  produces 

paresis  or  paralysis  of  the  right  arm,  whilst  the  left  arm, 
deprived  of  the  guidance  of  that  centre,  becomes  apraxic. 

2.  A  lesion  of  the  left  internal  capsule,  where  the  commissural 

fibres  are  uninjured,  causes  right-sided  hemiplegia,  without 
left-sided  apraxia. 

3.  A  lesion  of  the  corpus  caUosum,  or  of  the  left  centrum  ovale 

implicating  callosal  fibres,  will  cause  left-sided  apraxia 
(from  loss  of  the  guidance  of  the  left  arm-centre  over  the 
right),  whilst  the  right  hand  is  neither  paralysed  nor 
apraxic, 

4.  A  lesion  of  the  right  frontal  lobe  may  interrupt  the  callosal 

fibres  passing  from,  the  left  to  the  right  arm-centre  without 
injuring  those  of  the  pyramidal  path  from  the  right  centre 
to  the  left  hand.  In  such  a  case  we  have  a  left-sided 
apraxia  from  a  right-sided  lesion. 


CHAPTER   VIII 

DISORDERS   OF  ARTICULATION 

It  is  necessary  to  distinguish  clearly  between  speech  and  articula- 
tion.    Speech  is  a  cortical  function,  articulation  is  mainly  bulbar, 

Disordered  articulation,  or  dysarthria,  signifies  difficulty  in  per- 
forming the  co-ordinated  muscular  movements  necessary  for  the 
production  of  the  consonants  and  vowels  which  go  to  form  syllables 
and  words. 

In  simple  dysarthria  there  is  no  affection  of  the  cortical 
centres  or  paths  which  are  concerned  in  the  processes  of  speech 
proper.  A  patient,  for  example,  who  has  advanced  bulbar  palsy, 
even  when  he  is  unable  to  articulate  a  single  word,  is  not,  strictly 
speaking,  speechless.  He  is  inarticulate,  which  is  quite  a  difierent 
thing.  His  mental  speech-processes  remain  normal,  he  can  still 
express  himself  fluently  in  written  speech,  and  he  is  able  to  under- 
stand everything  he  hears  or  sees. 

The  peripheral  mechanism  of  vocal  speech  is  partly  musical 
(or  voiced),  consisting  in  vibration  of  the  approximated  vocal 
cords.  It  is  also  partly  consonantal  (or  voiceless),  consisting  in 
the  co-ordinated  action  of  numerous  muscles  of  the  lips,  tongue, 
palate,  and  pharynx.  The  term  "  articulation  "  is  specially  applied 
to  the  mechanism  of  consonantal  pronunciation. 

To  test  a  patient's  power  of  articulation,  we  listen  to  his 
ordinary  conversation,  or  we  ask  him  to  read  aloud  a  passage 
from  a  book  or  newspaper,  and  notice  how  he  pronounces  his 
words.  Then,  if  he  shows  any  abnormality  in  cormection  with 
particular  consonants,  we  ask  him  to  repeat  "  catch "  words, 
chosen  so  as  to  present  special  difficulties,  e.g.  "  British  consti- 
tution," "  bibUcal  criticism,"  "  West  Register  Street,"  "  hippopo- 
tamus," "  Burgess's  fish-sauce  shop,"  &c. 

Difficulties  of  articulation  are  the  result  of  defects,  consisting 


no  NERVOUS    DISEASES 

either  in  paralysis  or  inco -ordination,  of  certain  groups  of  muscles 
in  the  lips,  tongue,  palate,  pharynx,  or  larynx.  The  underlying 
defect  may  either  be  in  the  bulbo-muscular  neurones  (comprising 
the  pontine  and  medullary  nuclei,  the  peripheral  motor  nerves  and 
the  muscles),  or  it  may  be  due  to  supra-nuclear  affections  in  the 
cortico-bulbar  neurones,  at  some  point  between  the  higher  speech- 
centres  and  the  bulbar  nuclei.  Or  it  may  be  due  to  ataxia  of  the 
organs  of  speech. 

Infra-nuclear  and  Nuclear  Affections  of  Articulation. — 
Articulation  may  be  impaired  as  a  result  of  paralysis  of  any  of  the 
motor  nerves  or  nuclei  supplying  the  articulative  muscles. 

Unilateral  hypoglossal  paralysis  (as  in  the  case  of  a  business  man 
shown  in  Fig.  81,  in  whom  this  nerve  was  divided  by  a  stab  in  the 
neck  dealt  by  a  discharged  employe)  produces  motor  paralysis 
followed  by  atrophy  of  the  corresponding  half  of  the  tongue.  The 
paralysed  half -tongue  feels  to  the  patient  as  if  he  had  a  foreign 
body  in  his  mouth.  This  makes  his  articulation  clumsy,  lisping  and 
indistinct,  especially  in  the  case  of  hnguo-dental  (S,  Z,  Th)  and  of 
anterior  hnguo-palatal  consonants  (T,  D,  L,  R).  But  after  a  few  days 
the  patient  becomes  accustomed  to  the  feeling  of  his  palsied  half- 
tongue,  and  his  articulative  difficulty  to  a  large  extent  disappears. 
Facial  palsy,  from  its  affection  of  the  lips,  renders  labials  (P,  B) 
and  labio-dentals  (F,  V)  indistinct,  especially  so  when  the  palsy 
is  bilateral. 

Bilateral  paralysis  of  the  palate,  e.g.  post-diphtheritic  paralysis, 
congenital  cleft  palate,  and  syphihtic  perforation  of  the  palate, 
all  produce  the  same  articulative  difficulty,  inasmuch  as  the  nasal 
cavity  cannot  be  shut  off  from  the  mouth.  As  a  result  the  voice 
is  nasal,  and  certain  consonants  are  altered  (B  becomes  M,  D  be- 
comes N,  K  becomes  Ng,  and  so  on),  so  that  articulation  as  a 
whole  is  indistinct.  This  indistinctness  of  articulation  is  increased 
when  the  patient  stoops  forwards  :  it  diminishes  or  even  disappears 
on  lying  with  the  head  thrown  backwards,  since  in  the  latter 
position  the  soft  palate  tends  to  fall  back  by  its  own  weight  and 
shuts  off  the  naso-pharynx.^ 

1  Schlesinger,  Neurologisches  Gentralblatt,  1906,  p.  50. 


DISOEDERS    OF    ARTICULATION  111 

Total  paralysis  of  the  palate  is  also  associated  with  difl&culty 
in  deglutition,  especially  with  fluids,  which  during  the  act  of  swallow- 
ing regurgitate  into  the  naso-pharynx  and  escape  through  the 
anterior  nares. 

Unilateral  paralysis  of  the  recurrent  laryngeal  nerve  renders 
the  voice  hoarse,  by  paralysing  one  vocal  cord,  and  so  inter- 
fering with  the  phonation  of  vowels,  but  not  with  the  articu- 
lation of  consonants.  If  the  vagus  root  be  affected  at  its  point  of 
exit  from  the  medulla,  the  soft  palate  is  often  paralysed  on  the 
same  side  (see  later.  Cranial  Nerves).  But  unilateral  palatal 
palsy,  unlike  bilateral,  does  not  affect  the  articulation  of  consonants. 

Articulation  may  also  become  indistinct  from  disease  of  the 
bulbar  nuclei — so-called  glosso-labio-laryngeal  paralysis,  or  bulbar 
folsy.  In  this  disease  there  is  a  diffuse,  progressive  weakness  of 
the  muscles  of  articulation,  with  atrophy  and  fibrillary  tremors  of 
the  muscle  fibres,  especially  those  of  the  tongue  and  hps.  Articula- 
tion becomes  more  and  more  indistinct,  sahva  dribbles  from  the 
patient's  trembhng  hps,  and  in  advanced  cases  there  is  interfer- 
ence with  swallowing  and  coughing.  If,  as  is  often  the  case, 
bulbar  palsy  is  an  upward  extension  of  an  amyotrophic  lateral 
sclerosis,  there  may  be  a  concomitant  muscular  atrophy  and 
fibrillary  tremor  in  the  muscles  of  the  upper  hmbs,  especially 
in  the  intrinsic  hand  muscles.  Owing  to  affection  of  the  pyra- 
midal tracts,  there  is  also  exaggeration  of  the  deep  reflexes  and 
general  spasticity,  especially  of  the  lower  hmbs. 

There  is  a  form  of  myopathy — the  facio-scapulo -humeral  type 
of  Landouzy  and  Dejerine,  in  which  the  facial  muscles  are 
atrophied.  This  affection  is  a  bilateral  one  and  the  patient's 
lower  hp  protrudes  in  a  characteristic  fashion  which  has  been 
termed  the  "  tapir  "  type  of  lip.  He  has  also  a  peculiar  "  trans- 
verse "  smile.  In  severe  cases  of  this  disease  the  articulation  of 
labial  consonants  becomes  impaired  just  as  it  does  in  double 
facial  palsy. 

Myasthenia  gravis,  when  it  affects  the  bulbar  muscles,  repro- 
duces all  the  features  of  bulbar  palsy,  with  this  difference,  that 
the  paralysis  varies  in  its  degree  from  time  to  time,  becoming 


112  NEEVOUS    DISEASES 

accentuated  by  fatigue.  After  a  period  of  rest  a  patient  so 
affected  may  resume  with  normal  articulation,  but,  if  he  continues 
to  speak,  his  muscles  gradually  become  exhausted,  and  his  articula- 
tion becomes  more  and  more  indistinct.  Not  only  the  lips  and 
tongue,  but  the  ocular  muscles,  the  muscles  of  mastication  and 
various  muscles  of  the  trunk  and  Hmbs,  show  evidence  of  temporary 
paralysis  or  fatigue,  and  ultimately  the  patient  succumbs  to  fatigue 
of  his  respiratory  muscles. 

Articulative  Ataxia. — There  are  some  diseases  in  which  articu- 
lation becomes  indistinct,  not  from  paralysis  of  the  muscles  but 
from  ataxia. 

In  Friedreich's  ataxia,  for  example,  the  articulation  becomes 
slow,  thick,  and  clumsy,  and  the  patient  talks  as  if  he  had  a 
foreign  body  in  his  mouth,  so  that  his  speech  has  been  aptly 
termed  the  "  hot-potato  "  speech.  The  pitch  of  the  voice  in  this 
disease  may  vary  from  word  to  word,  and  in  advanced  cases  a 
certain  degree  of  mental  feebleness  is  often  superadded. 

In  laryngeal  tabes  where  the  larynx  is  affected  by  ataxy  the 
voice  is  tremulous,  and  when  a  tabetic  patient  has  ataxia  of 
the  tongue  his  articulation  becomes  laboured.  This  lingual  trouble 
in  tabes  is  often  associated  with  a  peculiar  constant  rolling  move- 
ment of  the  tongue  on  the  floor  of  the  mouth,  even  when  the 
patient  is  not  speaking.  The  patient  often  has  an  annoying 
subjective  sensation  in  his  tongue,  as  if  it  were  covered  with 
blotting-paper,  which  he  tries  to  get  rid  of  by  the  restless  rolling 
of  his  tongue. 

Supra-nuclear,  or  Cortico-bulbar  Affections  of  Articulation. 
— Articulation  may  be  affected  where  the  upper  or  cortico-nuclear 
neurones  are  involved.  The  slurring  articulation  of  many  cases  of 
acute  alcoholic  intoxication  is  familiar  to  lay  observers,  being  especi- 
ally marked  in  the  pronunciation  of  labial  and  of  anterior  linguo- 
dental  consonants.  In  rare  instances  alcohoHc  dysarthria  persists 
for  days  after  the  alcoholic  celebration.  ToUmer  and  other  French 
authorities  ascribe  this  circumstance  to  cerebellar  intoxication. 
Many  alcoholic  patients  realise  their  own  articulative  difficulty, 
and  in  endeavouring   to   compensate   for  it,   they   utter   certain 


DISORDERS    OF    ARTICULATION  113 

words    with    a   deliberation   and    undue    emphasis    that   betrays 
them. 

Very  similar  to  the  alcohohc  articulation  is  that  of  general 
paralysis  of  the  insane.  But  the  typical  general  paralytic  shows 
also  a  characteristic  fibrillary  tremor  of  aU  the  muscles  around 
the  Ups  and  nose. 

Both  in  acute  alcoholism  and  in  general  paralysis  there  is 
often  a  tendency  to  choose  an  occasional  wrong  word,  or  to  mis- 
place syllables.  Such  defects  are  not  bulbar  but  cortical  in  origin. 
•In  the  later  stages  of  general  paralysis,  articulation  may  be  totally 
unintelligible,  reduced  to  a  mere  mumble. 

After  an  attack  of  right-sided  hemiplegia,  the  patient  is  often 
aphasic.  But  even  in  a  left-sided  hemiplegia  where  no  true 
aphasia  exists,  it  is  not  uncommon  to  find  a  temporary  change  in 
the  articulation,  which  loses  its  crispness,  and  becomes  a  little 
laboured  and  indistinct.  This  dysarthria  usually  passes  off  after 
a  few  days,  but  sometimes  persists  permanently,  varying  in  degree, 
especially  if  the  lesion  involves  the  lenticular  nucleus.  A  lesion  of 
the  left  lenticular  produces  greater  dysarthria  than  one  of  the  right 
nucleus.''  The  dysarthria  of  lenticular  disease  is  due  mainly  to 
spasticity. 

In  cases  where  a  patient  has  a  bilateral  hemiplegia  we  often 
meet  with  "  fseudo -bulbar  ^^  paralysis.  The  most  common  history 
is  that  there  have  been  one  or  more  hemiplegic  attacks,  all  confined 
to  the  same  side,  but  at  last  the  patient  has  an  attack  on  the 
opposite  side.  This  now  produces,  in  addition  to  the  classic  signs 
of  a  double  hemiplegia,  pseudo-bulbar  paralysis,  with  thick,  in- 
distinct articulation,  closely  resembhng  that  of  true  bulbar  palsy 
and  with  the  same  dribbling  of  saliva,  difficulty  in  swallowing, 
coughing,  &c.,  but  without  atrophy  or  fibrillary  tremors  of  the 
affected  muscles.  The  pseudo-bulbar  patient  is  emotionally 
irritable  ;  he  laughs,  or  more  often  cries,  on  shght  provocation, 
and,  unhke  the  subject  of  true  bulbar  paralysis,  he  is  generally 
somewhat    deficient    mentally.      There    is    usually   a    history    of 

^  Mingazzini,  Sulla  sintomatologia  delle  lesione  del  nucleo  lenticolare,  1902. 
2  Wilson,  "  Progressive  Lenticular  Degeneration,"  Brain,  1911. 

H 


114 


NEKVOUS    DISEASES 


successive   (more  rarely  of  simultaneous)   attacks   of  hemiplegia 
on  opposite  sides  of  the  body. 

Double  athetosis  is  a  disease  which  is  usually  congenital.  It 
is  characterised  by  wild  wriggling  and  twisting  movements  of  all 
the  limbs,  chiefly  on  attempted  voluntary  movements,  and  by 
grimacing  of  the  face,  together  with  spastic  rigidity  of  the  affected 
muscles  (see  Figs.  48  and  49)  There  is  generally  a  certain  degree 
of  mental  deficiency.  In  this  disease  articulation  is  often  affected. 
The  grimaces  of  the  face  and  of  the  tongue  muscles  interfere  con- 


FlG.  48. 


Fig.  49. 


Figs.  48  and  49. — Double  athetosis  in  a  girl  of  17.       The  patient  was  a  7^ 
mcnths'  child.     She  had  also  signs  of  stenosis  of  the  pulmonary  artery. 

siderably  with  articulation.  Moreover,  irregular  spasmodic  con- 
tractions of  the  diaphragm  and  other  respiratory  muscles  give 
the  voice  a  curiously  jerky  or  groaning  character,  due  to  sudden 
interruptions  of  breathing. 

Patients  suffering  from  disseminated  sclerosis  frequently  have 
a  peculiar  so-called  'staccato"  speech,  in  which  the  words  are 
enunciated  in  a  jerky  mincing  fashion,  very  difficult  to  describe, 
but  easy  to  recognise  once  it  has  been  heard.  This  is  sometimes 
called  the  "  scanning  "  speech,  from  its  fancied  resemblance  to 
the  scansion  of  Latin  or   Greek  verse. 


DISORDERS    OF    ARTICULATION  115 

In  •paralysis  agitans,  as  the  disease  advances,  the  patient's 
voice  becomes  thin,  feeble  and  reduced  almost  to  a  monotone, 
whilst  his  articulation,  like  his  gait,  acquires  a  "  festinant  "  char- 
acter. When  speaking,  he  begins  slowly,  but  towards  the  ends 
of  sentences  or  long  words  he  tends  to  hurry,  so  that  the  final 
syllables  are  pronounced  hastily.  Together  with  this  we  have  the 
characteristic  "  starched,"  expressionless  face,  the  Parkinsonian 
mask,  commencing  unilaterally  and  ultimately  becoming  bilateral. 

Severe  cases  of  cliorea  may  have  the  articulation  interfered 
with,  owing  to  sudden  violent  movements  of  the  face,  tongue,  and 
respiratory  muscles.  Speech  becomes  hesitating  and  jerky,  and 
in  very  bad  cases  the  voice  may  be  reduced  to  a  whisper. 

There  are  also  affections  of  articulation  due  to  functional 
cortical  disturbances.  Of  these  the  mcsfc  famihar  is  stammering, 
which  consists  in  a  want  of  co-ordination  between  the  vocal 
(laryngeal)  and  consonantal  (oral)  mechanisms  of  speech,  so  that, 
in  the  common  type,  the  patient  sticks  at  a  consonant,  which  he 
often  continues  to  repeat,  over  and  over  again,  before  he  finally 
succeeds  in  enunciating  the  rest  of  the  word.  He  misdirects 
his  energy  on  the  consonants,  instead  of  touching  them  hghtly 
and  passing  on  to  the  vowel  sounds.  Most  stammerers  lose  their 
stammer  when  they  sing,  their  attention  being  then  directed  to 
the  vocal  part  of  speech. 

A  rarer  variety  of  stammering  is  that  in  which  the  patient  sticks 
at  initial  vowels.  This  is  due  to  temporary  spasm  of  the  false 
vocal  cords,  and  the  patient  remains  with  his  mouth  wide  open 
until  the  spasm  relaxes,  when  his  words  suddenly  rush  forth  in  a 
hurried  stream  until  he  has  no  breath  left.  He  then  takes  another 
breath  and  the  precipitate  rush  again  occurs.^ 

Many  stammerers  acquire  various  tricks,  chiefly  through  their 
efiorts  to  overcome  the  stammer.   Thus  extra  noises  may  be  thrown 

1  Cathcart  has  pointed  out  that  this  variety  of  stammering  is  described 
in  Shakespeare's  "As  You  Like  It"  (Act  iii.  Scene  2)  as  follows:^ 

"  I  would  thou  couldst  stamnier,  that  thou  mightst  pour  out  this  con- 
cealed man  out  of  thy  mouth,  as  wine  comes  out  of  a  narrow-necked  bottle, 
either  too  mtich  at  once,  or  none  at  all.  I  prithee,  take  the  cork  out  of  thy 
mouth  that  I  may  drink  thy  tidings." 


116  ^  NEEVOUS    DISEASES 

in,  e.g.  sudden  inspiratory  grunting  or  whooping  noises,  or  the 
patient  may  make  grimaces  or  curious  contortions  of  the  Hmbs. 

This  leads  us  to  recall  the  various  articulative  tics  or  habit-spasms 
which  are  met  with  in  psychasthenic  patients,  either  in  conjunction 
with  stammering  or  independently  of  it,  and  these  may  be  of  the 
most  varied  character.  The  patient's  speech  may  be  interrupted 
by  weird  pharyngeal  barking  or  grunting  noises.  Or  the  articulation 
may  be  monosyllabic,  a  whole  breath  being  taken  for  each  syllable. 
Or,  again,  it  may  be  jumbled  up  in  the  most  extraordinary  ways, 
though  the  "  tiqueur  "  usually  interpolates,  now  and  then,  a  clearly 
articulated  sentence  or  phrase  amongst  the  other  unintelhgible 
ones.  Hysterical  aphonia  is  fairly  common,  and  can  usually  be 
recognised  by  the  history,  together  with  the  characteristic  laryngeal 
appearances.  We  also  meet  with  cases  of  hysterical  mutism,  where 
the  patient  does  not  utter  even  a  whispered  word. 

Deaf-mutes  are  the  patients  who  are  popularly  known  as 
"  deaf  and  dumb."  A  normal  child  learns  to  speak  by  imitating 
words  which  he  hears,  but  if  a  child  be  congenitally  deaf,  he 
does  not  learn  to  speak,  but  remains  deaf  and  dumb.  Moreover, 
if  he  is  born  with  normal  hearing,  but  subsequently  becomes  deaf, 
e.g.  from  middle  ear  disease  or  from  meningitis,  should  this  occur 
before  the  age  of  about  six  years,  he  usually  loses  his  power  of 
speech.  Deaf-mutes  can  generally  be  taught  to  speak  again  by 
the  oral  or  "  hp-reading  "  method,  where  the  child  imitates  the 
movements  of  his  teacher's  muscles  of  articulation  and  also  learns 
to  phonate,  though  usually  with  a  harsh,  discordant  voice.  But 
even  deaf-mutes  who  have  never  been  taught  to  speak  usually 
make  noises  of  some  sort  or  other,  often  pharyngeal  snorts  and 
grunts,  or  spluttering  labial  noises,  and  less  frequently  laryngeal 
sounds.  They  do  this  especially  when  excited.  This  was  the  case 
with  a  deaf-mute  who  used  to  make  weird  snorting  noises  when 
playing  football.  These  doubtless  helped  to  smite  terror  into  the 
hearts  of  the  opposite  side.  The  congenital  deaf-mute  is  usually 
brighter  and  more  clever  than  the  acquired  deaf-mute.  Deaf- 
mutes  generally  have  a  wonderful  command  of  gestures  and 
signs. 


DISOKDERS    OF    ARTICULATION  117 

The  dumbness  which  is  present  in  profound  degrees  of  idiocy 
is  not  an  articulative  difficulty,  but  a  true  speech  affection  due 
to  mal- development  of  the  cortical  speech-centres.  An  imbecile 
child  is  speechless  because  he  has  no  ideas  to  express ;  in  this 
respect  he  differs  from  the  deaf-mute,  who  is  often  bright  and 
intelligent. 

Certain  varieties  of  deficient  articulation  are  met  with  in 
children  or  in  adults  who  are  mentally  more  or  less  childish.  The 
condition  known  as  falling  consists  in  a  want  of  precision  in  the 
pronunciation  of  certain  consonants.  Thus  a  patient  may  substitute 
the  uvular  R  for  the  ordinary  linguo -palatal  R,  or  he  may  sub- 
stitute V  for  Th  or  W  for  R,  so  that  "  broken  reed  "  becomes 
"  b woken  weed."  Or,  again,  the  patient  may  substitute  Th  for  S 
and  is  then  said  to  lisp.  These  last  two  varieties  are  sometimes 
voluntarily  assumed,  as  a  fashionable  affectation,  by  young  men 
not  overburdened  with  brain  power.  More  serious  varieties  of  falling 
are  where  the  letter  L  is  replaced  by  some  other  consonant,  so 
that  "  elephant  "  may  be  pronounced  as  "  edephant,"  "  esephant," 
"  enephant,"  "  erephant,"  &c.  Still  worse  is  it  when  the  patient 
has  difficulty  with  K  or  G,  their  places  being  taken  by  T  and  D 
respectively. 

As  a  general  rule,  it  may  be  stated  that  lalling  on  a  single 
consonant  does  not  necessarily  indicate  defective  intellect,  whereas 
lalling  on  many  consonants,  if  the  patient  has  passed  the  age 
of  childhood,  should  arouse  the  suspicion  of  mental  deficiency, 
although  lalHng  is  a  normal  stage  in  the  process  of  learning  to 
speak. 

Finally,  there  is  the  condition  known  as  idioglossia,  where 
from  difficulty  in  pronouncing  his  consonants  a  child  retains  the 
correct  vowels,  but  substitutes  other  consonants  and  seems  to 
speak  a  new  language  of  his  own.  In  the  course  of  time  the 
child  usually  completely  outgrows  this  weakness. 


CHAPTER   IX 

CRANIAL    NERVES 

The  recognition  of  cranial  nerve  palsies  is,  diagnostically,  of  the 
utmost  importance,  nor  is  it  a  matter  of  such  diflB.culty  as  is 
commonly  imagined. 

First,  or  Olfactory  Nerves. — From  the  under  surface  of  the 
olfactory  bulb  on  each  side  there  arise  some  twenty  minute  nerves 
which  perforate  the  cribriform  plate  of  the  ethmoid  to  be  dis- 
tributed to  the  upper  part  of  the  nose.  To  test  the  sense  of  smell, 
we  direct  the  patient  to  close  his  eyes.  We  then  hold  aromatic 
substances,  such  as  oil  of  cloves,  peppermint,  or  asafoetida,  in 
front  of  each  nostril  in  turn,  closing  the  other  nostril  with  the 
finger.  Ammonia  or  acetic  acid  must  not  be  used  to  test  the 
sense  of  smell,  since  these  stimulate  the  fifth  nerve  (common  sensa- 
tion), and  may  produce  a  pungent  sensation  in  the  nose,  even 
when  the  sense  of  smell  is  lost. 

Anosmia,  or  loss  of  the  sense  of  smell,  is  sometimes  of 
diagnostic  value.  It  may  occur,  for  example,  in  congenital  absence 
of  the  olfactory  nerves,  in  some  frontal  tumours,  in  lesions  of  the 
olfactory  bulb  or  olfactory  tract,  in  injuries  of  the  anterior  fossa  of 
the  skull,  and  when  there  is  atrophy  of  the  olfactory  nerves  in  tabes. 
It  also  occurs  unilaterally  very  often  in  hysterical  hemiplegia  and 
is  then  associated  with  diminution  of  the  other  special  senses  on 
the  hemiplegic  side.  But  the  value  of  anosmia  as  a  symptom  is 
lessened  by  the  fact  that  numerous  local  obstructive  conditions 
in  the  nose  also  produce  loss  of  smell,  e.g.  nasal  polypi  or  even  a 
simple  cold  in  the  head. 

Parosmia,  or  perverted  sense  of  smell,  is  always  cortical  in 
origin.  Various  subjective  hallucinations  of  smell  occur  not  only 
in  mental  disease  but  also  in  gross  lesions  of  the  uncinate  gyrus, 
which  is  the  cortical  olfactory  centre.     But  here  again  local  nasal 

118 


CRANIAL    NERVES 


119 


conditions  may  also  cause  olfactory  sensations,  e.g.  the  unpleasant 
odour  perceived  by  a  patient  suffering  from  empyema  of  the 
antrum  of  Highmore,  from  wliich  horribly  offensive  pus  is  escaping 
into  the  nose.  On  the  other  hand,  in  ozsena  from  chronic  atrophic 
rhinitis  the  offensive  smell  is  not  perceived  by  the  patient,  though 
it  is  painfully  evident  to  his  neighbours. 

Paroxysmal  parosmia,  preceded  by  a  disagreeable  feeling  of 
irritation  at  the  root  of  the  nose,  and  sometimes  followed  by 
violent  sneezing  and  by  sudden  secretion  of  nasal  mucus,  may 
occur  as  a  nasal  crisis  in  tabes. ^ 


Fig.  50. — Diagram  of  pons  and  medulla,  showing  cranial  nerves. 

Second,  or  Optic  Nerve. — This  contains  not  only  visual  fibres, 
but  also  the  afferent  fibres   or  the  pupillary  reflex. 

We  have  already  referred  to  the  course  of  the  visual  path  from 
retina  to  cortex  (Fig.  23,  p.  38).  In  testing  vision  we  should 
determine  visual  acuity  by  means  of  test  types  at  a  fixed  distance, 
such  as  six  metres.  Using  Snellen's  tjrpes,  of  which  the  largest 
should  be  readable  at  sixty  metres,  and  the  smallest  at  six  metres, 
we  direct  the  patient  to  read  the  letters  from  above  downwards. 
If  his  vision  is  normal  he  will  be  able  to  read  the  smallest  type  at 
six  metres.  His  visual  acuity  is  then  represented  as  V  =  |-.  But  if 
he  can  only  read  down  as  far  as  the  type  which  ought  to  be  visible  at 
thirty  metres,  then  V  =  ^'q.  Each  eye  should  be  tested  separately, 

^   Klippel  and  Lhermitte,  Semaine  Medicale,  Feb.  17,  1909. 


120 


NERVOUS    DISEASES 


the  test  types  being  well  illuminated  and  the  patient  standing 
with  his  back  to  the  light.  When  the  visual  acuity  is  much  im- 
paired, the  patient  may  not  see  even  the  largest  type,  but  can  only 
count  fingers  at  a  short  distance,  or  perhaps  can  only  tell  light 
from  darkness.  Temporary  diminution  of  visual  acuity  may 
occur  in  myasthenia  gravis.-^ 

Hemeralo'pia,  or  day-blindness,  is  a  condition  in  which  the  power 
of  vision  is  bad  during  the  day  or  in  a  bright  light,  whilst  the 
patient  sees  better  in  a  dim  light.  The 
phenomenon  is  not  uncommon  in  tobacco 
amblyopia,  where  there  is  usually  present 
a  central  scotoma  for  green  and  red.  The 
hemeralopia  is  probably  due  to  the  fact 
that  a  bright  light  rapidly  fatigues  the 
retina  and  also,  by  producing  pupillary 
contraction,  causes  the  peripheral  part  of 
the  retina  to  be  less  in  use  than  the 
central,  whereas  in  a  dim  light  the  pupil 
dilates  and  the  unaffected  peripheral  por- 
tion of  the  retina  comes  into  play. 

Nyctalopia,  or  night-blindness,  where 
the  patient  becomes  almost  blind  at  dusk 
or  in  a  dim  light,  is  associated  with  vari- 
ous conditions,  of  which  the  most  inter- 
esting is  congenital  retinitis  pigmentosa,  a 
disease  easily  recognised  on  ophthalmoscopic  examination.  It 
also  occurs  to  a  lesser  degree  in  certain  cases  of  "  cortical " 
cataract,  where  the  lenticular  opacity  acts  as  a  permanent 
diaphragm. 

Colour  vision  is  most  conveniently  tested  by  means  of  Holmgren's 
wools.  These  are  thrown  on  a  table  well  lit  by  daylight,  and  the 
patient  is  given  one  particular  test-skein  of  wool  which  is  kept 
separate  from  the  heap,  and  told,  not  to  name  the  colour,  but  to 
match  it,  selecting  from  the  heap  of  coloured  skeins  all  those  which 
are  like  the  test-skein,  whether  lighter  or  darker  in  shade.  The 
^  Tilney  and  Mitchell  Smith,  Neurographs,  1911,  vol.  i.  p.  178. 


Fig.  51. — Lateral  view  of 
brain-stem  with  cra- 
nial nerves. 


CRANIAL    NERVES  121 

patient  is  given  a  pale  green  test-skein.  If  his  colour  vision  is 
normal,  lie  will  pick  out  all  the  pale  greens  correctly,  but  if  he  is 
red-green  colour-bhnd  he  will  select  a  grey  or  straw-coloured  skein. 
Congenital  red-green  colour-blindness  is  the  commonest  variety. 
Yellow-blue  colour-blindness  is  less  common.  If  a  patient  be 
totally  colour-blind  he  will  confuse  with  the  test-skein  all  those 
of  similar  brightness,  no  matter  what  their  colour  may  be. 

The  size  of  the  field  of  vision  in  each  eye  is  of  great  importance, 
and  for  its  accurate  measurement  a  perimeter  is  required.  This, 
however,  is  a  large  and  expensive  apparatus.  For  clinical  purposes 
the  following  method  is  sufficient,  presuming  that  the  physician's 
own  visual  fields  are  normal.  The  physician  sits  exactly  opposite 
the  patient,  about  a  yard  away  from  him,  and  tests  each  eye 
separately.  To  test  the  patient's  right  eye  direct  him  to  cover  up 
his  left  and  to  gaze  steadily  at  the  physician's  left  eye.  Meanwhile 
the  physician  closes  his  own  right  eye  and  looks  steadily  at  the 
patient's  pupil,  watching  that  the  patient's  eye  does  not  wander 
from  the  fixation  point.  Then,  holding  his  own  left  hand  in 
a  plane  midway  between  himself  and  the  patient,  and  beginning 
almost  at  arm's-length,  he  brings  his  hand  inwards  from  the 
patient's  ear  towards  the  middle  Hne,  meanwhile  moving  his  own 
fingers.  If  the  patient's  visual  field  is  normal,  he  will  catch  sight 
of  the  moving  fingers  at  th«  same  time  that  the  physician  does  so. 
If  he  does  not,  that  visual  field  is  contracted  and  the  physician 
then  brings  his  moving  fingers  inwards  until  the  patient  does  catch 
sight  of  them.  In  this  way  we  test  both  the  upper  and  lower 
quadrants  of  the  field  on  the  temporal  and  nasal  sides,  in  turn. 
If  we  find  the  visual  field  diminished  in  one  or  other  eye,  it  is  well 
to  take  a  careful  perimetric  chart. 

We  may  find  a  central  scotoma  or  blind  patch  in  one  or  both 
visual  fields.  This  is  detected  by  attaching  a  small  white  object 
to  the  end  of  a  thin  rod  and  holding  it  in  the  centre  of  the  visual 
field,  midway  between  one's  own  and  the  patient's  eye.  In  this 
situation  it  is  not  seen  by  the  patient.  "We  gradually  move  the 
white  object  radially  outwards  in  various  directions  imtil  the 
patient  catches  sight  of  it.     Central  scotoma  may  occur  in  various 


122 


NERVOUS    DISEASES 


organic  diseases  of  the  optic  nerve  or  retina,  such  as  early  optic 
atrophy,  central  retinal  hsemorrhage,  &c.,  or  it  may  result,  in  a 
minor  degree,  from  obstruction  to  central  vision,  e.g.  by  central 
opacities  in  the  lens  or  cornea.  It  may  also  occur,  as  a  temporary 
phenomenon,  in  some  cases  of  migraine.      Such  conditions  are  easy 


JlUfht  £y^_ 


Fig.  52. — Crossed  amblyopia,  in  a  case  of  hysteria. 


RiyhtEy^ 


00  100 


Fig.  53. — Right  homonymous  hemianopia,  in  a  case  of  softening  of  the  left 

occipital  lobe. 

of  recognition.  Central  colour  scotoma  to  red  and  green  (detected 
in  a  similar  fashion  with  coloured  objects)  together  with  deficient 
visual  acuity,  is  highly  suggestive  of  tobacco  amblyopia.  In  such 
cases,  besides  a  history  of  chronic  excess  in  tobacco,  we  look  for 
corroborative   signs   such  as   fine  tremor  of   the   hands,    cardiac 


CRANIAL    NERVES  123 

irregularity,  cardiac  pain,  &c.  An  almost  identical  amblyopia  may 
also  occur  from  chronic  alcoholism. 

The  visual  field  may  be  concentrically  contracted.  This  con- 
dition is  sometimes  due  to  optic  atrophy,  the  field  being  reduced 
to  a  small  area  surrounding  the  fixation-point,  so  that  the  patient 
looks  at  the  outer  world  as  though  through  a  narrow  tube.  More 
commonly  concentric  contraction  of  the  visual  field  occurs  in 
hysteria,  the  field  on  the  hemiplegic  side  of  the  body  being  more 
contracted  than  that  on  the  other  side  (Fig.  52).  Temporary 
contraction  of  the  visual  field  may  occur  in  myasthenia  gravis. 
Less  frequently  a  cortical  lesion  of  the  angular  gyrus,  not  impli- 
cating the  subjacent  optic  radiation  (Fig.  23),  causes  a  similar 
concentric  contraction  of  both  fields,  more  marked  in  the  eye  of 
the  side  opposite  to  that  of  the  brain  lesion.  This  is  somewhat 
clumsily  named  crossed  amhlyofia,  but,  as  previously  observed, 
it  is  much  commoner  in  hysteria  than  in  organic  brain  disease, 
and  in  hysteria  it  is  frequently  associated  with  diminution  or  loss 
of  other  special  senses  on  the  side  of  the  more  contracted  field 
whose  colour  sense  is  frequently  lost  (achromatopsia).  Hysterical 
amblyopia  is  unknown  to  the  patient,  and  is  only  discovered  on 
examination  by  the  physician. 

Hemianopia  (Fig.  53)  means  bUndness  of  half  the  visual  field, 
right  or  left  as  the  case  may  be,  from  causes  other  than  retinal 
disease.  It  usually  affects  the  visual  field  of  both  eyes,  and  is  due 
to  a  lesion  of  the  visual  fibres  at  or  behind  the  O'ptic  chiasma. 
Such  chiasmic  lesions  may  result  from  pressure  by  tumours, 
syphihtic  or  inflammatory  afiections  of  the  basi-sphenoid,  from 
tumours  of  the  brain  or  of  its  membranes,  and  especially  from 
pituitary  tumours,  as  in  acromegaly.  We  have  already  considered 
the  signs  of  lesions  of  the  optic  tracts,  and  it  is  convenient  here 
to  recall  the  effects  of  lesions  of  the  optic  chiasma. 

(A)  If  the  lesion  be  in  the  central  part  of  the  chiasma,  inter- 
rupting the  decussating  optic  fibres  (belonging  to  the  nasal  halves 
of  both  retinse),  there  is  bhndness  in  the  outer  half  of  each 
visual  field  : — hi-temporal  hemiano'pia  (Fig.  54).  This  sometimes 
occurs  in  pituitary  tumours. 


124  NERVOUS   DISEASES 

(B)  If  the  lesion  be  situated  at  one  or  other  lateral  extremity 
of  the  chiasma,  it  will  interrupt  merely  the  non-decussating  fibres 
of  the  optic  nerve  and  optic  tract  on  that  side,  causing  unilateral 
nasal  hemianopia  in  the  corresponding  eye.  To  produce  bilateral 
nasal  hemianopia  there  must  be  two  separate  lesions,  one  at  each 
end  of  the  chiasma,  a  condition  which  very  seldom  occurs.  A 
lesion  involving  the  central  part  of  the  chiasma  and  extending  to 
one  or  other  side  (Fig.  54,  A  plus  B)  will  produce  the  sum  of  these 
two,  namely  bi-temporal  hemianopia  'plus  unilateral  nasal  hemi- 

R.  Optic  Tract.  L.  Optic  Tract. 


R.  Eye.  L.  Eye. 

Fig.  54. — Diagram  of  course  of  visual  fibres  in  optic  chiasma. 
(Hamilton.) 

anopia,  i.e.  total  blindness  of  one  eye  with  temporal  hemianopia 
of  the  other. 

(C)  A  lesion  of  the  left  optic  tract  behind  the  chiasma  produces, 
as  already  seen,  hemianopia  in  the  right  halves  of  both  fields 
of  vision. 

(D)  A  lesion  of  one  optic  nerve  simply  causes  blindness  in  the 
corresponding  eye. 

In  rare  cases  we  may  have  a  quadrantic  hemianopia  in  which 
only  one  quadrant  (instead  of  one-half)  of  both  visual  fields  is  blind. 
This  is  generally  due  to  a  lesion  Hmited  to  part  of  the  cortical  half- 
vision  centre  in  the  cuneate  lobule  and  lingual  gyrus.  The  calcarine 
fissure  divides  the  half-vision  centre  into  an  upper  and  a  lower  part. 


CRANIAL    NERVES  125 

A  lesion  above  the  calcarine  fissure,  i.e.  in  the  cuneate  lobule, 
causes  blindness  of  the  lower  quadrant,  whilst  a  lesion  below  the 
calcarine  fissure,  i.e.  in  the  lingual  gyrus,  causes  blindness  of  the 
upper  quadrant  of  the  corresponding  half-fields.^ 

The  optic  discs  and  retinae  should  be  examined  with  the 
ophthalmoscope  in  every  case  of  nervous  disease.  The  most  im- 
portant conditions  to  look  for  are  optic  neuritis  and  optic  atrophy. 
O'ptic  neuritis  occurs  in  numerous  pathological  conditions  within 
the  skull,  especially  in  intra-cranial  tumours  and  in  tuberculous 
meningitis.  But  it  also  occurs  in  nephritis,  in  lead  poisoning,  in 
diabetes,  and  in  severe  ansemia  ;  and  these  four  common  conditions 
must  always  be  excluded  before  we  diagnose  gross  intra-cranial 
disease.  We  may  also  meet  with  optic  neuritis  in  certain  cases  of 
cervical  myelitis.  Oftic  atrofhy  may  occur  primarily,  as  in  tabes 
and  disseminated  sclerosis,  or  it  may  be  a  secondary  post-neuritic 
process.  Sometimes  it  follows  a  retro-hulbar  neuritis,  whether 
occurring  spontaneously,  or  in  disseminated  sclerosis,  or  in  chronic 
alcohol  or  tobacco  poisoning.  Pallor  of  the  temporal  halves  of  the 
optic  discs  is  often  an  early  sign  of  disseminated  sclerosis.  The 
combination  of  optic  atrophy,  blindness,  and  mental  deficiency 
occurs  in  the  amaurotic  family  idiocy  of  Tay  and  Sachs,  an  affection 
of  certain  Jewish  children,  coming  on  in  infancy.  In  these  cases, 
on  ophthalmoscopic  examination  there  is  a  characteristic  cherry- 
red  spot  seen  at  the  macula  lutea,  due  to  local  csdema  and  atrophy 
of  the  retina,  whereby  the  vascular  choroid  shines  through.  Apart 
from  optic  neuritis  and  optic  atrophy,  we  must  be  on  the  lookout 
for  other  pathological  conditions  of  the  fundus,  such  as  choroiditis, 
albuminuric  retinitis,  tubercle  of  the  choroid,  occlusion  of  the 
central  retinal  artery,  retinal  haemorrhage,  &c. 

It  must  be  remembered  that  a  patient  may  have  severe  optic 
neuritis  without  any  impairment  of  vision.  Optic  atrophy,  on  the 
other  hand,  causes  the  visual  field  to  contract  concentrically  to  a 
greater  or  less  extent,  whilst  the  visual  acuity  diminishes  and 
ultimately  the  eye  becomes  blind.     The  atrophy  of  retro-bulbar 

^  Henschen,  Le  Centre  cortical  de  la  Vision.  Internat.  Med.  Congress, 
Paris,  1900. 


126  NERVOUS    DISEASES 

neuritis  often  produces  central  scotoma  from  affection  of  the  papillo- 
macular  bundle  of  optic  nerve  fibres.  Scotoma  is  often  the  first 
sign  of  retro-bulbar  neuritis,  long  before  atrophy  is  visible  by 
the  opbtbalmoscope. 

Third,  Fourth,  and  Sixth  Nerves. — It  is  convenient  to  study 
together  these  three  nerves  which,  between  them,  innervate  all 
the  voluntary  muscles  of  the  eye.  The  distribution  of  each  is  as 
follows  : — The  third  nerve  (oculo-motorius)  supplies  all  the  external 
ocular  muscles  except  two  : — the  superior  oblique  supplied  by  the 
fourth  nerve,  and  the  external  rectus  supphed  by  the  sixth.  It 
also  supphes  the  voluntary  part  of  the  levator  palpebrae  superioris 
(the  involuntary  part  being  supphed  by  the  cervical  sympathetic), 
and  it  contains  fibres  which  indirectly,  through  the  cihary  ganglion 
and  short  ciliary  nerves,  supply  the  non-striated  sphincter  pupillse  and 
ciliary  muscle.  The  fourth  nerve  (patheticus)  supphes  the  superior 
oblique  alone,  the  sixth  nerve  (abducens)  the  external  rectus  alone. 

Until  comparatively  recently,  the  motor  nucleus  for  the  pupil 
was  generally  considered  to  be  located  in  the  third  nucleus,  and 
in  a  special  part  of  it  near  its  anterior  end  (the  so-called  Edinger- 
Westphal  nuclei,  situated  close  to  the  middle  hne,  one  on  each 
side,  consisting  of  small  nerve  cells  embedded  amongst  the 
larger  cells  of  the  oculomotor  nucleus).  To  explain  the  occur- 
rence of  loss  of  the  light-reflex  various  theoretical  lesions 
were  assumed,  sometimes  in  these  Edinger  -  Westphal  nuclei 
(Bernheimer  ^),  sometimes  in  Meynert's  fibres  leading  from  the 
anterior  corpora  quadrigemina  to  the  supposed  pupillary  centre 
in  the  third  nucleus.  But  against  the  first  of  these  theories, 
cases  have  been  recorded  of  tumour  of  the  mid-brain  completely 
destroying  the  oculomotor  nuclei  and  so  producing  ophthalmoplegia 
externa,  and  yet  the  pupillary  reflex  still  remained  (Biancone,^ 
Jacobsen  ^).  Moreover,  total  ophthalmoplegia,  internal  and  ex- 
ternal, has  occurred  without  any  affection  of  the  Edinger- 
Westphal  nuclei  (Monakow  ^).  Further,  degeneration  of  Meynert's 
fibres    has   not   been   demonstrated,    even    in   cases  of   fabes    or 

^  V.  Graefe's  Archiv,  1897.  ^  Rivista  di  Freniatria,  1899. 

'^  Deutsche  Med.  Wochensch.,  1900. 

*  Gehirn-pathologie,  4te  Aufl.  1905,  s.  1053. 


CRANIAL    NERVES 


127 


general  paralysis  where  loss  of  the  pupillary  light-reflex  is  one 
of  the  commonest  clinical  phenomena.  Lastly,  experimental 
and  clinical  evidence  (Piltz,^  Bach  ^)  has  shown  that  the  ciliary 
ganglion  is  the  peripheral  motor  nucleus  controlling  the  sphincter 
pupillse,  and  Marina,^  in  a  series  of  twenty-eight  cases  of  tabes  and 
general  paralysis  exhibiting  the  Argyll-Robertson  pupil,  found 
this  ganglion  invariably  degenerated.  In  one  of  them  where  the 
Argyll-Robertson  phenomenon  was  confined  to  one  eye,  the  ciliary 


Corporob  Quxxjdrigerrvinaj 


Effere;ni-  \ 

InMbitoryFvbres  fram, 
Brairvto  CiLuxry  Ganglion 


HI  Nucleus 

-£xb.  GenLcxdaLiiBoob/ 


'^^^   (4)  CUijctry  GangLLorv. 

^^    ■  PupiZ>-corustrictingFUjres. 


Jj.EYB 


Fig.  55. — Diagram  of  the  path  of  the  pupil-reflex  (modified  from  Bach). 

ganglion  was  degenerated  on  that  side  alone,  the  ganglion  of  the 
other  side  being  normal.  It  is  therefore  probable  that  degenera- 
tion renders  the  ciliary  ganglion  inexcitable  to  the  stimulus  of 
light,  whereas  it  can  still  respond  to  the  stronger  stimulus  of  volun- 
tary impulses  transmitted  along  the  third  nerve.  The  connection 
between  the  anterior  corpus  quadrigeminum  and  the  third  nerves 
is  vid  the  fasciculus  sublongitudinahs.^ 

The  Pupil. — We  note  the  size  of  the  pupil,  both  in  a  bright 
and  in  a  dim  light,  and  we  observe  whether  the  pupils  are  equal  in 

1  Neicrologisches  Centralhlatt,  1903.         ^  Zeitsch.  fur  Augenheilkunde,  1904. 

^  Annali  di  Nevrologia,  1901. 
*  Majano,  Monatschrift  fiir  Psychiatrie  und  Neurologie,  1903,  Bd.  xiii.  Heft  1. 


128  NERVOUS    DISEASES 

diameter.  Abnormal  dilatation  of  tlie  pupil  {mydriasis)  is  often 
present  in  anaemia  and  neurastlienia,  but  it  may  occur,  on  one  or 
both  sides,  in  organic  nervous  disease.  Mydriasis  may  be  either 
paralytic,  from  paralysis  of  tbe  spbincter  pupillae,  as  in  disease  of 
the  third  nerve  or  cihary  ganghon,  or  it  may  be  irritative,  as 
when  due  to  stimulation  of  the  dilator  pupillse.  It  also  occurs 
when  optic  atrophy  has  caused  bhndness,  and  is  then  due  to  the 
absence  of  visual  impressions.  Myosis  or  abnormal  contraction  of 
the  pupil  occurs  in  pontine  haemorrhage,  probably  from  irritation 
of  inhibitory  fibres  leading  from  the  brain  to  the  ciliary  gangha. 
It  is  also  present  in  many  cases  of  tabes,  as  well  as  in  certain 
cases  of  disease  of  the  cervical  region  of  the  cord  (notably  in 
syringomyeha)  from  interruption  of  the  pupU-dilating  fibres." 
Myosis  is  also  caused  by  iritis  and  by  the  irritation  of  foreign 
bodies  in  the  cornea,  and  a  transient  myosis  occurs  for  a  day  or 
so  after  excision  of  the  Gasserian  ganglion  ^  (see  Fig.  55). 

Variations  in  the  size  of  the  pupil  may  also  be  the  result  of 
mydriatic  drugs,  either  locally  instilled  (atropine,  homatropine, 
cocaine)  or  taken  internally  (beUadoima),  whilst  other  drugs  are 
myotics,  either  local  (eserine,  pilocarpine)  or  internal  (opium, 
jaborandi). 

The  outhne  of  the  pupH  should  be  carefully  examined.  Some- 
times, instead  of  being  circular,  it  is  oval  or  irregularly  polygonal. 
Such  variations  have  an  important  diagnostic  value.  For  if  we 
exclude  congenital  malformation  such  as  coloboma,  operative  pro- 
cedures such  as  iridectomy,  and  disease  such  as  iritis  and  synechise, 
then  it  may  be  taken  as  a  general  rule  that  irregularity  of  the  pupiJs 
signifies  either  tabes,  general  paralysis,  or  old  syphilis,  the  lesion 
being  either  in  the  short  cihary  nerves  or  in  the  ciliary  ganghon 
itseH.  Ectopia  pu-pillce  is  a  condition  in  which  the  pupil  is  not 
in  the  centre  of  the  iris.  Sometimes  it  occurs  in  lesions  of  the 
mid -brain ;  *  in  other  cases,  however,  it  appears  to  have  no 
pathological  significance.     Irregularity  of  the  pupil  can  be  pro- 

1  Bach,  Zeitschrift  filr  Augenheilkunde,  1904,  s.  105. 
2  See  later.  Cervical  Sympathetic,^.  335.     ^  H.  M.  Da^^ies, Brain,  1907,  p.  265. 
4  s_  A.  K.  Wilson,  Brain,  1906,  p.  524. 


CRANIAL    NERVES  129 

duced  experimentally  by  stimulation  or  division  of  the  short 
cihary  nerves.  Each  eye  must  be  tested  separately,  noting  the 
effect  on  the  pupil  of  shading  and  uncovering,  first  the  same  eye 
and  then  the  opposite  eye. 

The  "pupillary  reflex  to  light  should  always  be  observed.  Nor- 
mally the  iris  contracts  when  Hght  falls  on  the  retina,  whether  of 
the  same  eye  (direct  reflex)  or  of  the  opposite  eye  (consensual 
reflex).  The  light-reflex  depends  upon  the  integrity  of  a  reflex  arc, 
whose  afferent  limb  is  the  peri-macular  fibres  of  the  retina  and  optic 
nerve,  whose  intermediate  station  is  in  the  mid-brain  and  whose 
efferent  limb  passes  through  the  third  nerve  and  cihary  ganglion 
to  the  pupillary  sphincter  (Fig.  55). 

If  the  healthy  pupil  be  strongly  illuminated  and  examined  with 
a  magnifying  lens  (say  x  10),  we  observe  that  it  is  not  stationary 
but  in  a  continuous  state  of  fine  irregular  movement,  slight 
alternate  narrowing  and  widening,  varjdng  both  in  rhythm  and 
amplitude.  This  normal  pupillary  unrest  '^  must  not  be  confounded 
with  hippus,  which  is  a  pathological  condition  consisting  in  rhythmic 
clonic  contractions  of  the  iris,  regular  in  their  periodicity,  much 
coarser  in  range,  and  visible  to  the  naked  eye.  Loss  of  the  normal 
pupillary  mirest  is  always,  pathological,  and  may  be  one  of  the 
earhest  signs  of  organic  affection  of  the  reflex  visual  path,  e.g.  in 
tabes  or  general  paralysis. 

Loss  of  reaction  to  Hght  occurs  in  optic  atrophy,  in  paralysis 
of  the  third  nerve,  and  in  degeneration  of  the  cihary  ganghon. 
Loss  of  the  hght-reflex  with  preservation  of  contraction  during 
accommodation  for  near  objects — ^the  classic  Argyll  -  Robertson 
phenomenon — occurs  typically  in  tabes  and  in  general  paralysis 
of  the  insane.  Marina  has  shown  this  to  be  associated  with  de- 
generation of  the  ciliary  ganglion.  It  also  occurs  in  blindness  from 
optic  atrophy.  In  the  early  stages  of  optic  atrophy  the  pupil  of 
the  affected  eye  may  contract  to  light  fairly  well  for  a  moment, 
but  under  continued  exposure  it  dilates  again,  unlike  a  healthy 
pupil."-^     If   this    phenomenon   be    associated   with    diminution    of 

1  Hubner,  Archiv  fiir  Psychiatric,  1906,  Band  41,  s.  1016. 

2  Gunn,  Brit.  Med.  Journal,  1907:  p-  353. 


130  NERVOUS    DISEASES 

visual  acuity  or  with  failure  to  distinguish  between  red  and  green 
in  the  centre  of  the  visual  field,  we  should  be  suspicious  of  early- 
optic  atrophy  (even  though  the  optic  disc  be  normal  in  appear- 
ance), which  in  many  cases  is  due  to  commencing  disseminated 
sclerosis.  Wernicke's  hemiopic  'pupillary  reaction,  in  certain  cases 
of  hemianopia,  is  absence  of  pupillary  contraction  when  a  ray  of 
light  is  thrown  on  the  blind  side  of  the  retina.  It  signifies  a  lesion 
of  the  visual  path  behind  the  chiasma,  and  below  or  at  the  cor- 
pora quadrigemina.  In  retro -quadrigeminal  hemianopia,  where  the 
lesion  is  anyw^here  between  the  corpora  quadrigemina  and  the 
visual  cortex,  the  pupillary  reaction  is  normal  (Fig.  23,  p.  38). 

The  reaction  of  the  pupil  to  accommodation  is  the  contraction  of 
the  pupil  which  occurs  when  the  patient  converges  the  eyes  to  look 
at  a  near  object.  We  test  this  by  holding  a  finger  close  to  the 
patient's  face,  first  teEing  him  to  look  at  some  distant  object, 
and  then  suddenly  to  look  at  the  finger.  If  he  is  blind,  he 
can  nevertheless  converge  by  attempting  to  look  at  his  own  finger. 
In  paralysis  of  the  third  nerve  there  is  total  immobility  of  the 
corresponding  pupil,  both  to  hght  and  on  convergence.  Loss  of  the 
contraction  on  accommodation  with  preservation  of  the  hght-reflex 
— a  condition  the  converse  of  the  Argyll-Robertson  phenomenon 
— is  not  uncommon  after  diphtheria,  and  is  often  accompanied 
by  other  evidences  of  post-diphtheritic  neuritis,  such  as  paralysis 
of  external  ocular  muscles  or  of  the  palate,  loss  of  knee-jerks, 
&c.  Paradoxical  pupillary  reaction  is  when  the  pupil  dilates 
instead  of  contracting  on  accommodation.  This  phenomenon, 
which  is  not  uncommon  in  tabes  (occurring,  according  to  Pilcz,  in 
40  per  cent,  of  cases),  can  be  demonstrated  in  two  ways.  Firstly, 
energetic  voluntary  closure  of  the  eye  .produces  a  synergic  con- 
traction of  the  pupil,  which  dilates  again  when  the  eye  is  re- 
exposed  to  light.  Secondly,  if  we  tell  the  patient  to  depress  the 
upper  hd  whilst  we  forcibly  prevent  it  from  descending,  we  see 
the  pupil  contract,  whilst  the  eye  moves  upwards  and  out- 
wards to  get  under  cover  of  the  upper  hd.  The  reaction  of  the 
pupil  to  painful  stimulation  of  the  skin  of  the  neck,  causing  the 
pupil  to  dilate,  is  important  with  regard  to  the  cervical  sympathetic. 


CRANIAL    NERVES 


131 


It  is  often  absent  in  the  early  stages  of  tabes.  A  psychical 
dilatation  of  the  pupil  also  occurs,  temporarily,  under  the  influence 
of  lively  emotion,  such  as  fear,  intense  interest,  sexual  orgasm, 
&c.  The  pupil  may  even  contract  or  dilate  when  the  individual 
thinks  of  a  dark  object  or  a  luminous  one. 

Let  us  now  consider  paralysis  of  external  ocular  muscles. 

To  detect  paralysis  of  the  ocular  muscles,  having  first  examined 
the  pupils,  noting  their  size  and  any  irregularity  of  outhne,  and 
having  tested  their  reaction  to  light  and  on  accommodation,  we 
then  ask  the  patient  to  follow  our  finger  with  his  eye,  making  him 
look  alternately  up,  down,  to  the  right  and  left,  and  making  him 


bif.O 


Sup.R 


Sup.R 


Jnf.O 


Sup.O.  Inf.R.  InF.R.  Sup.O. 

Fig.  .'5G. — N.  Bishop  Harman's  chart  to  show  (1)  Movements  of  ocular  muscles, 
and  (2)  Position  of  false  image  in  paralysis. 

1  (rt)  Rectangular  movements.  The  arrows  point  to  the  direction  in  which  the  eye  is  turned 
by  each  muscle. 
Qj)  Rotation.  Put  a  match,  head  upwards,  on  each  of  the  dotted  lines  indicating  tlie 
vertical  meridians.  "Muscles  that  rotate  eye  inwards  turn  the  match-head  tovvards 
nose  (Sup.  Rectus  and  Sup.  Oblique) ;  those  that  rotate  it  outwards  turn  match  in  the 
opposite  direction  (Inf.  Oblique  and  Inf.  Rectus). 

2.  Put  matches  on  diagram  again.  The  match  will  represent  the  true  image.  The  four  rays 
marked  Sup.  R.,  Inf.  R.,  Sup.  O.,  and  Inf.  O.  will  represent  the  relative  position  (in 
vertical  and  lateral  displacement  and  tilting)  of  the  false  image  produced  in  paralysis 
of  each  of  these  muscles.  In  paralysis  of  Int.  or  Ext.  Rectus  the  false  image  will  run 
vertically  through  the  corresponding  arrow-head. 

converge.     Meanwhile  we  observe  whether  there  be  any  squint, 
deficient  movement  in  any  direction,  diplopia,  or  nystagmus. 

If  an  individual  muscle  is  paralysed,  there  is  diplopia,  squint, 
and  deficiency  of  movement  of  the  affected  eye  towards  the  direc- 
tion of  traction  of  the  affected  muscle.  Fig.  56  is  Bishop  Harman's 
diagram  indicating  the  action  of  the  individual  muscles.  A  simple 
rule,  worth  remembering  in  all  cases  of  ocular  paralysis,  is  that  the 
affected  eye  is  displaced  (by  the  unopposed  antagonists)  in  a  direction 
opposite  to  the  direction  of  traction  of  the  paralysed  muscle,  whilst 
the  false  image,  seen  by  the  affected  eye,  is  displaced  in  the  direction 


132 


NERVOUS   DISEASES 


of  traction  of  the  paralysed  muscle.  Figs.  57  and  58  are  Werner's 
well-known  "  memoria  teclinica,"  showing  the  position  of  the  false 
image  in  the  various  ocular  paralyses.  Fig.  57  shows  the  position 
of  the  false  image  in  paralysis  of  any  of  the  recti ;  Fig.  58  in 
paralysis  of  the  oblique  muscles.  For  example,  Fig.  57  shows 
that    in    diplopia    from    paralysis    of    the    left    inferior    rectus, 

(1)  the  false  image  is  on  the  right  of  the  true  {i.e.  it  is  crossed) ; 

(2)  the  false  image  has  its  upper  end  inchned  towards  the  true ; 

(3)  the  false  image  is  lower  than  the  true ;  and  (4)  the  diplopia 
occurs  on  downward  movement  of  the  eyes.     To  test  diplopia  we 


Left    supr. 
Rectus 


Left   infr. 
Rectus 


Right    supr. 
Rectus 


Right  infr. 
Rectus 


Left  infr.- 
oblique 


Left  supr. 
oblique     - 


Right  infr. 
oblique 


Right  supr. 
oblique 


Fig.  57. 


Fig.  58. 


Figs.  57  and  58.— "Werner's  "artificial  memory"  for  the  double  images  in  ocular 
paralyses  {Ophthalmic  Review,  1886).  Fig.  57  shows  the  position  of  the 
images  in  paralysis  of  the  recti  muscles.  Fig.  58  in  paralysis  of  the  oblique 
muscles.  The  "dotted  lines  indicate  "false"  images,  the  thick  black  lines 
"  true  "  images. 


use  a  long,  lighted  candle,  at  a  distance  of  about  three  yards  from 
the  patient,  holding  it,  first,  exactly  opposite  the  patient  and 
moving  it  gradually  from  side  to  side  and  then  from  above  down- 
wards. One  of  the  patient's  eyes  is  covered  with  a  red  and  the 
other  with  a  green  glass,  to  differentiate  the  two  images,  and  the 
patient  has  to  tell  us  the  relative  position  of  the  red  and  of  the 
green  candle.  It  is  necessary  to  ensure  that  the  patient  keeps 
his  head  fixed  during  the  process  of  testing.  The  false  image  is 
that  seen  by  the  paralysed  eye,  the  true  image  by  the  sound  one. 
Diplopia  is  a  more  delicate  test  than  paralytic  squint,  for  where 


CRANIAL    NERVES  133 

there  is  slight  paresis  of  an  ocular  muscle  there  may  be  no  notice- 
able squint,  and  yet  the  diplopia  may  be  quite  appreciable  to  the 
patient.  To  detect  a  paralytic  squint  we  direct  the  patient  to  follow 
our  finger,  moving  it  laterally  from  side  to  side,  and  then  vertically 
up  and  down,  and  observe  whether  there  is  deficiency  of  movement 
of  one  or  both  eyes  in  any  particular  direction  or  directions. 

Nystagmus  is  an  involuntary  rhythmic  tremor  of  the  eyeballs, 
generally  bilateral  and  symmetrical.  The  movement  consists  of 
an  oscillation  usually  horizontal,  from  side  to  side,  but  sometimes 
vertical  or  even  rotatory.  Nystagmus  may  be  either  oscillating 
(where  the  movements  to  both  sides  are  equal  in  range  and  of 
equal  speed)  or  rhythmic,  the  commoner  type,  where  both  move- 
ments are  equal  in  range  but  the  one  is  fast  and  the  other  slow. 
In  most  cases  nystagmus  occurs  only  when  the  eyes  are  voluntarily 
moved  to  an  extreme  degree  either  laterally  or,  less  commonly, 
vertically ;  in  rhythmic  horizontal  nystagmus  the  rapid  jerk  is  to 
the  side  towards  which  the  eyes  are  directed.  But  sometimes, 
especially  in  the  rotatory  variety,  nystagmus  occurs  when  the  eyes 
are  directed  straight  forward.  In  cases  where  an  ocular  muscle 
has  been  paralysed  but  is  in  process  of  recovery,  if  we  make  the 
patient  look  steadily  in  a  direction  which  necessitates  the  active 
movement  of  the  formerly  paralysed  muscle,  slight  rhythmic 
nystagmus  may  develop,  analogous  to  tremulousness  of  the  hand 
after  carrying  a  heavy  weight.  Nystagmus  occurs  in  various 
organic  diseases,  notably  in  disseminated  sclerosis,  Friedreich's 
ataxia  and  cerebellar  disease.  It  is  present  also  in  certain  patients 
who  have  become  more  or  less  blind  (though  in  complete  blindness 
the  movement  is  more  often  a  slow  rolling  of  the  eyes),  also  in 
albinism,  and  a  well-recognised  form  is  miner's  nystagmus,  due  to 
persistent  ocular  strain  in  a  dim  light.  Miner's  nystagmus  is 
oscillating,  generally  vertical  and  accompanied  by  spasm  of 
the   levator    palpebree. 

Another  variety  is  aural  or  vestibular  nystagmus.  This,  together 
with  violent  vertigo,  may  be  produced  experimentally  in  healthy 
subjects  by  syringing  the  drum  of  the  ear  with  water,  either 
distinctly  above  or  distinctly  below  the  temperature  of  the  body. 


134  NERVOUS    DISEASES 

Bdrany  -^  regards  this  nystagmus  as  a  result  of  convection  currents 

in  the  endolymph  produced  by  warming  or  cooling  of  the  labyrinth. 

The  presence  of  such  thermic  nystagmus  can  be  used  as  a  test  of 

the  integrity  of  the  vestibular  nerve.     The  objective  phenomena 

vary  according  to  the  position  of  the  patient's  head.     Thus,  for 

example,  if  the  patient  be  standing  up,  with  the  head  turned 

face  downwards,  and  if  the  left  ear  be  irrigated  with  cold  water, 

the  nystagmus  which  is  produced  is  horizontal  in  type  with  the 

quick  jerk  to  the  left  and  most  marked  when  the  patient  looks 

towards  the  left  side.      Meanwhile  the  head  and  eyes,  and  even 

the  trunk,  tend  to  rotate  strongly,   around  the  long  axis  of  the 

body,  towards  the  right  side.     If  the  patient's  head  be  erect  when 

his  left  ear  is  syringed  with  cold  water,  the  nystagmus  is  rotatory 

in  type  and  to  the  right,  and  the  forced  movement  of  the  head  and 

trunk  is  a  lateral  bending  towards  the  left  side.      If  hot  water  be 

used  instead  of  cold,  the  direction  of  nystagmus  and  of  forced 

movement  of  the  head,  eyes,  and  trunk  is  in  each  case  reversed.^ 

There  is  also  a  rare  congenital  affection  known  as  nystagmus- 

myoclonus,  in  which,  together  with  nystagmus,  commonly  of  the 

lateral  oscillating  variety,  there  are  involuntary  jerking  movements 

of  the  limbs  or  trunk.     These  movements  are  aggravated  by  cold  or 

by  tapping  the  muscles,  but  can  be  controlled  by  an  effort  of  will. 

The  deep  reflexes  are  often  exaggerated,  and  it  is  not  unusual  to 

have  other  co-existing  deformities,  such  as  hypospadias,  flat-foot, 

facial  asymmetry,  persistent  branchial  cleft,  &c.^ 

Nystagmus  can  be  produced  in  a  normal  person  by  placing  him  on  a 
rotating  stool  and  spinning  him  rapidly  around  the  long  axis  of  his  own 
body ;  in  such  a  case,  if  the  stool  be  suddenl}^  stopped,  a  temporary  after- 
nystagmus  appears,  horizontal  and  rhythmic,  the  rapid  phase  of  the  nystag- 
mus being  in  the  opposite  direction  from  the  j^revious  rotation.  If  a 
patient  who  already  has  a  horizontal  nystagmus  be  similarly  revolved 
around  his  own  long  axis,  on  suddenly  stopping  the  rotation  we  find  tliat  the 
original  nystagmus  towards  the  direction  of  rotation  has  temporarily  ceased 
whilst  that  in  the  opposite  direction  is  exaggerated.*  In  such  a  case,  the 
experimental  after-nystagmus  lias  for  the  time  over-compensated  the  pre- 
existing nystagmus. 

'  Centralblatt  fiir  Augenheilkunde,  August  1905. 

2  Scott,  Lancet,  June  11,  1910. 

^  Lenoble  and  Aubineau,  Revue  de  Medecine,  July  16,  1906. 

*  Cassirer  and  Loeser,  Neurologisches  Centralblatt,  1908,  s.  252. 


CRANIAL    NERVES 


135 


We  are  now  in  a  position  to  recognise  the  signs  of  paralysis 
of  any  of  the  ocular  nerves.  In  a  case  of  complete  third  nerve 
paralysis  (Figs.  59  and  60)  there  is  ptosis  or  drooping  of  the  upper 
lid,  from  paralysis  of  the  levator  palpebree,  with  over-action 
of  the  frontalis  on  that  side,  so  that  the  eyebrow  stands  higher 
than  normal.  In  hysterical  ptosis  (Fig.  61),  on  the  other  hand, 
there  is  no  over-action  of  the  frontalis,  nor  is  there  in  the  ptosis  of 
myasthenia  gravis,  where  the  frontalis  is  usually  partially  paralysed 
as  well.  In  third  nerve  paralysis  there  is  also  external  strabismus 
from  unopposed  action  of  the  external  rectus,  and  there  is  inabihty 


Fig.  59. 


I'IG.  60. 


Fig.  59. — Total  paralysis  of  right  third  uerve  from  syphilitic  disease. 
Fig.  60. — The  same  patient,  the  right  eyelid  being  passively  lifted  to  show  the 
external  strabismus  and  dilatation  of  pupil  on  the  paralysed  side. 

to  move  the  eye  upwards,  directly  downwards,  or  directly  inwards, 
although  a  slight  downward  and  inward  movement  can  be  executed 
by  the  superior  oblique.  The  pupil  is  dilated  owing  to  paralysis  of  the 
sphincter  iridis,  and  does  not  contract  either  to  light  or  on  attempted 
accommodation.  Complete  paralysis  of  the  third  nerve  is  less 
common  than  is  a  partial  paralysis,  affecting  one  or  more  muscles. 
Weakness  of  the  internal  recti  sometimes  occurs  in  exophthalmic 
goitre  (constituting  Moebius's  sign).  We  make  the  patient  look 
upwards  to  the  ceiling  and  then  ask  him  to  look  at  the  tip  of  his 


136 


NERVOUS    DISEASES 


own  nose,   when  we  observe  that  only  one  eye  converges,   the 
other  eye  becoming  divergent. 

Paralysis  of  the  Fourth  Nerve   produces  paralysis  of  the 
superior  oblique  muscle  of  the  corresponding  eye.     This  muscle 


Fig.  G1. — Case  of  left-sided  hysterical  ptosis  in  a  woman  of  25,  sliowing 
absence  of  frontalis  over-action  on  paralysed  side.  The  area  on  the  left 
side  of  the  head,  neck,  trunk  and  shoulder,  within  the  black  line,  was 
totally  auEesthetic  to  all  forms  of  stimuli.  There  was  loss  of  smell  and  taste 
on  the  left  side :  contraction  of  the  left  visual  field  and  diminution  of 
hearing  in  the  left  ear.  The  figure  also  shows  the  presence  of  "dermo- 
graphism." The  patient's  name  having  been  traced  on  the  chest  with  the 
head  of  a  pin,  a  hard,  cord-like  pattern  was  produced,  capable  of  being 
photographed. 

has  a  threefold  action  :  it  turns  the  anterior  pole  of  the  eye 
downwards  and  outwards  and  at  the  same  time  rotates  its  vertical 
meridian  slightly  inwards  (see  Fig.  56).  The  deficiency  of  move- 
ment is  difficult  to  see,  and  the  paralysis  is  recognised  mainly 
by  the  characteristic  diplopia  which  occurs  when  the  patient  gazes 
in  the   direction  in   which  the  superior  oblique  ought  to   come 


CRANIAL    NERVES  137 

into  action,  i.e.  downwards  and  outwards.  When  the  patient  looks 
horizontally  forwards  or  upwards  there  is  no  diplopia.  But  when  he 
looks  downwards  and  outwards,  diplopia  appears,  the  false  image 
standing  lower  than  the  true,  and  having  its  upper  end  tilted 
towards  the  other  (Fig.  58).  The  false  image  also  appears  to  the 
patient  nearer  to  him  than  the  true,  the  reason  for  which  is  obscure. 
Moreover  the  patient  feels  giddy,  especially  when  he  looks  down- 
wards, as  in  walking  downstairs,  and  he  habitually  inclines  his 
head  forward  and  towards  the  sound  side. 

Paralysis  of  the  Sixth  Nerve  is  particularly  easy  to  recognise. 


I'IG.  62.  Fig.  62a. 

Case  of  paralysis  of  the  left  sixth  nerve,  of  six  weeks'  duration,  in  a  girl 
of  20,  the  subject  of  juvenile  tabes. 

Fig.  62  shows  the  normal  movement  of  both  eyes  on  looking  to  the  right. 
Fig.  62a  shows  attempted  movement  of  eyes  to  the  left.      The  left  eye  is 
arrested  at  the  mid-position. 

There  is  merely  paralysis  of  the  external  rectus,  with  inability  to 
turn  the  eye  outwards  beyond  the  mid-point,  all  other  movements 
being  normal  (Figs.  62  and  62a),  and  there  is  diplopia  on  looking 
outwards.  In  old  cases  in  which  contraction  of  the  non- paralysed 
internal  rectus  has  supervened,  an  internal  strabismus  results. 

Sometimes  an  external  ocular  muscle  is  attacked  by  rheumatic 
myositis,  which  causes  an  ocular  palsy  of  benign  form.  The  muscle 
most  frequently  thus  affected  is  the  external  rectus. 

Ocular  paralyses  differ  in  type  according  as  they  are  due  to 
a  supra-nuclear  lesion  (between  the  second  frontal  gyrus  and  the 
ocular  nuclei),  a  nuclear  lesion  in  the  mid-brain,  or  an  infra-nuclear 
lesion  of  the  individual  nerves  such  as  we  have  just  described. 

Ocular   paralysis   from  a  supra-nuclear  lesion  never  attacks  a 


138  NERVOUS    DISEASES 

single  ocular  muscle  or  even  a  single  eye.  On  the  contrary,  associ- 
ated muscles  of  both  eyes  are  affected.  The  common  type  of 
paralysis  from  a  destructive  lesion  at  or  above  the  internal  capsule 
is  one  in  which  the  patient  loses  the  power  of  turning  both  eyes 
towards  the  contra -lateral  side.  Therefore  the  unopposed  anta- 
gonists draw  both  eyes  over  towards  the  side  of  the  lesion  ;  this  is 
called  conjugate  deviation.  In  certain  cases  of  conjugate  deviation, 
although  the  patient  can  no  longer  turn  his  eyes  voluntarily  to 
one  side,  say  the  right,  he  can  do  so  reflexly  by  fixing  some  object 
directly  in  front  with  his  eyes,  this  object  being  then  moved  to- 
wards the  right  or  the  patient's  head  being  passively  rotated  to 
the  left.'-  Curiously  enough,  conjugate  deviation  upwards  or 
downwards  does  not  occur  from  a  paralytic  lesion  of  the  internal 
capsule,  unless  a  bilateral  lesion  is  present.  In  supra-nuclear 
lesions  reflex  nystagmus  is  still  preserved.  Barany  ^  has  shown  that 
reflex  nystagmus  can  be  produced  in  normal  individuals  in  two 
ways.  Firstly,  there  is  oftic  nystagmus,  produced  by  making  the 
patient  watch  a  rapidly- moving  landscape  when  looking  out  of  the 
window  of  a  railway  carriage,  or  by  making  him  watch  a  series  of 
vertical  bars  on  a  horizontally  revolving  cylinder.  Secondly,  there 
is  vestibular  nystagmus,  produced  either  by  rapid  rotation  of  the 
individual  on  a  revolving  chair  (rotation  to  the  right  producing 
horizontal  nystagmus  to  the  left  and  vice  versd),  or  by  syringing 
the  ear  with  cold  water,  stimulation  of  the  right  ear  producing 
nystagmus,  partly  horizontal  but  mainly  rotatory,  to  the  left  and 
vice  versd  (see  above,  p.  134).  If  the  vestibular  nerve  be  diseased, 
reflex  vestibular  nystagmus  is  abolished.^ 

Shew  deviation  of  the  eyes  occurs  in  certain  lesions  of  the 
lateral  lobe  of  the  cerebellum  or  of  its  middle  peduncle.  Thus  in 
a  woman  with  a  fatal  haemorrhage  in  the  right  half  of  ths  cere- 
bellum and  pons,  the  right  eye  was  directed  downwards  and 
inwards,  and  the  left  eye  upwards  and  outwards, 

A  nuclear  lesion  of  the  third,  fourth,  or  sixth  nuclei  in  the  floor 
of  the  Sylvian  aqueduct  may  be  partial  or  complete,  and  the  type 

1  Bielschowsky,  Miinchener  medizinische  Wochenschrift,  1903,  s,  1666. 

2  Baraay,  ibid.,  1907,  s.  1072, 


CRANIAL    NERVES  ]39 

of  ocular  palsy  whicli  results  is  called  nuclear  ophthalmoplegia. 
In  some  cases  the  fibres  for  the  ciliary  ganglia  or  the  gangha  them- 
selves or  short  ciliary  nerves  to  the  internal  ocular  muscles  (iris 
and  ciliary  muscle)  are  alone  affected,  and  not  the  external  muscles 
of  the  globe.  The  result  is  ophthalmoplegia  interna,  in  which  the 
pupils  are  dilated  and  immobile  both  to  light  and  on  convergence. 
This  condition  may  be  unilateral  or  bilateral,  according  as  the  ciliary 
ganglia  or  short  cihary  nerves  are  affected  on  one  or  both  sides. 
It  often  occurs  as  a  transient  result  of  post-diphtheritic  neuritis. 
Ophthalmoplegia  externa  is  a  nuclear  disease  of  the  Sylvian  aqueduct 
affecting  numerous  external  ocular  muscles,  generally  of  both  eyes 
and  often  symmetrically.  A  fairly  common  type  is  where  the 
power  of  upward  rotation  of  the  eyes  is  lost,  lateral  movements 
being  still  possible.  Ophthalmoplegia  externa  usually  occurs  alone, 
less  commonly  it  is  associated  with  the  internal  variety.  When  both 
varieties  are  combined  we  have  total  ophthalmoplegia,  in  which 
the  eyes  are  fixed  and  motionless,  the  pupils  being  immobile, 
both  varieties  of  reflex  nystagmus  (optic  and  vestibular)  being 
lost,  and  the  patient  can  look  in  any  particular  direction  only 
by  facing  his  head  that  way  en  bloc.  Nuclear  ophthalmoplegia, 
especially  external  ophthalmoplegia,  may  be  associated  with  motor 
paralysis  of  the  limbs  if  the  lesion  extends  ventrally  and  impli- 
cates one  or  other  pyramidal  tract,  or  it  may  be  associated  Avith 
involuntary  tremors  if  the  lesion  affects  the  red  nucleus  or  rubro- 
spinal tract  (Fig.  15,  p.  23). 

Sometimes  it  is  possible  to  differentiate  between  a  nuclear  and 
an  infra-nuclear  ocular  lesion.  In  the  case  of  paralysis  of  the  sixth 
nucleus  in  the  pons,  there  is  not  merely  weakness  of  the  external 
rectus  of  the  same  side,  as  in  paralysis  of  the  sixth  nerve  trunk, 
but  in  addition  the  internal  rectus  of  the  opposite  eye  is  paralysed, 
so  that  conj  agate  movement  of  both  eyes  towards  the  affected 
side  is  impaired.  The  vreakness  of  the  contra-lateral  internal 
rectus  is  only  in  connection  with  its  associated  movement  with 
the  external  rectus  of  the  ipso-lateral  eye.  This  is  proved  by 
the  fact  that,  in  paralysis  limited  to  the  sixth  nucleus,  both 
internal  recti  can  still  act  normally  during  convergence.     Again, 


140  NERVOUS    DISEASES 

since  the  facial  motor  root  loops  round  the  sixth  nucleus  within 
the  pons,  a  lesion  of  the  sixth  nucleus  is  not  infrequently 
accompanied  by  facial  paralysis  on  the  same  side.  The  sixth 
nucleus  is  essentially  an  oculogyre  centre,  turning  both  eyes  to 
the  corresponding  side,  and  therefore  controlHng  not  only  the 
external  rectus  of  the  ipso -lateral  side,  but  also  the  internal 
rectus  of  the  contra-lateral  side. 

With  regard  to  the  diagnosis  between  nuclear  and  infra-nuclear 
paralysis  of  the  third  nerve,  if  in  a  doubtful  case  the  orbicularis 
oculi  is  found  to  be  affected  together  with  the  external  ocular 
muscles,  then  the  lesion  is  in  the  region  of  the  nucleus,  since  the 
orbicularis  is  innervated  by  a  group  of  cells  which  are  in  anatomical 
proximity  to  the  oculomotor  nucleus  (but  which  really  belong  to 
the  facial). 

Mendel's  theory  ^  assumed  tliat  these  cells  belonged  to  the  oculomotor 
nucleus  and  reached  the  orbicularis  through  the  facial,  but  Bishop  Haiman^ 
has  shown  that  all  the  facial  muscles,  from  orbicularis  oculi  downwards^  are 
innervated  from  the  group  of  cells  comprising  the  facial  nucleus,  the  ujjper 
end  of  this  group  extending  as  high  as  the  oculomotor,  and  the  lower  end 
reaching  to  the  level  of  the  hypoglnssal. 

Sometimes  transient  ocular  palsy  affects  the  third  nerve  in 
whole  or  in  part,  recurring  in  the  same  eye  without  apparent 
cause  at  intervals  of  weeks  or  months,  and  clearing  up  com- 
pletely between  the  attacks.  This  condition,  known  as  Charcot's 
migraine  ophtalmopUgique,  is  generally  associated  with  headache, 
most  intense  in  the  eye  and  forehead  of  the  affected  side,  and 
with  vomiting.  Its  pathology  is  obscure ;  probably  some  cases 
are  due  to  an  inflammatory  affection  of  the  meninges  at  the  point 
where  the  third  nerve  pierces  them  to  enter  the  sphenoidal  fissure. 
This  is  all  the  more  probable  inasmuch  as  the  first  division  of  the 
fifth  nerve,  which  traverses  the  sphenoidal  fissure,  is  often  simul- 
taneously affected,  with  the  result  that  there  is  blunting  of  sensa- 
tion in  its  area  of  distribution. 

Now  and  then  we  meet  with  congenital  ptosis,  in  which  there 
is  paralysis  of  the  superior  rectus  and  levator  palpebrse  superioris 

^  International  Med.  Congress,  Washington,  1887,  vol.  5,  p.  311. 
2   Transactions  of  Ophthalpiological  /Society,  1903,  p.  356. 


CRANIAL   NERVES 


141 


of  one  eye.  In  some  of  these  cases,  although  the  patient  cannot 
raise  his  upper  lid  voluntarily,  yet,  curiously  enough,  the  lid  is 
jerked  up  when  certain  jaw  movements  are  made,  particularly  when 
the  patient  throws  into  action  the  external  pterygoid  muscle  of  the 
same  side,  in  depressing  the  lower  jaw  towards  the  opposite  side. 

This  so-called  "  jaw-winking  "  movement  has  been  shown  by 
Harman  to  be  the  survival  of  a  movement  in  fishes  whereby,  when 
the  mouth  is  opened  for  breathing  or  eating,  the  gill  swings  open. 
In  man  the  pterygoid  and  orbicularis  oculi  muscles  are  homologous 


TirsiI)iMiisix)rh 


{  SecondLDivisicmi  - 


^M^\ 

>^ 

Great  OccipiboOb 

Mk 

\ 

Nerve. 

If  ^^ 

\ 

SmjoJlOccipibah 
^^     Nerve 

IKy 

] 

AurCcularBranch, 

^""/i 

cfVcugue  and. 
Nervas  inte/'me.diALs 

■s^  GrealAvricvJUxr 

>d      //i 

JServe. 

ThirdbDijvhSWTV  - 


Arubl 


CerviccxLJfervpS 
Fig.  63. — Cutaneous  supply  of  head  (modified  from  Frolise). 

with  the  deep  and  superficial  muscles  of  the  branchial  arch  of  the 
fish's  spiracle,  and  when  the  one  is  contracted  the  other  tends  to 
relax  and  "  the  weak  levator,  taking  advantage  of  the  quiescence 
of  its  too  powerful  opponent,  lifts  the  eyelid." 

Jaw- winking  movements  generally  disappear  before  adult  life. 

The  Fifth  or  Trigeminal  Nerve  has  a  most  extensive  dis- 
tribution, the  main  points  of  which  are  as  follows  : — The  nerve 
consists  of  two  distinct  parts,  sensory  and  motor.  The  sensory  root, 
the  one  on  which  is  the  Gasserian  ganghon,  divides  below  the 
ganglion  into  three  divisions,  of  which  the  first  two  are  entirely 
sensory.     The  motor  root  courses  beneath  the  Gasserian  ganglion, 


142 


NERVOUS   DISEASES 


and  then  joins  the   third  division,  which  thus  becomes  a  mixed 


nerve. 


The  ftrst  or  ophthalmic  division  passes  through  the  sphenoidal 
fissure  into  the  orbit  and  supphes  the  eyeball  and  lachrymal  gland, 
the  conjunctiva  (except  that  of  the  lower  hd),  the  skin  of  the  fore- 
head and  scalp  up  to  the  vertex  (Fig.  63),  the  mesial  part  of  the 
skin  of  the  nose,  and  the  mucous  membrane  of  the  upper  part  of 
the  nasal  cavity.      It  also  contains  efferent  pupil-dilating  fibres 


Gasseria.7v 


Gemculate  GamfUon] 


longiie. 


Stylomastoid  forame/L 
-Posmrior Auricular 


Olosso  plLoryngeaL 


Fig.  04. — Diagram  of  trigeminal,  facial,  and  glosso-pharyngeal  nerves, 
showing  course  of  taste  fibres. 

derived  from  the  cervical  sympathetic,  joining  it  at  the  Gasserian 
ganglion,  and  going  to  the  iris  (Fig.  55). 

The  second  or  superior  maxillary  division  passes  through  the 
foramen  rotundum  across  the  spheno-maxillary  fossa  to  the  infra- 
orbital canal.  In  the  spheno-maxillary  fossa  it  is  connected  with 
Meckel's  ganglion,  which  gives  off  amongst  other  branches  the 
Vidian  nerve.  This  latter  runs  backwards  to  join  the  facial  nerve, 
the  posterior  end  of  the  Vidian  being  named  the  great  superficial 
petrosal  (Fig.  64).  The  superior  maxillary  division  supplies  the 
skin  of  the  upper  lip,  the  side  of  the  nose  and  adjacent  part  of  the 
cheek,  the  lower  eyelid  and  part  of  the  temple.    It  also  supplies  the 


CRANIAL   NERVES  143 

conjunctiva  of  the  lower  lid,  the  upper  teeth,  the  mucous  membrane 
of  the  upper  lip,  the  upper  part  of  the  cheek,  upper  jaw,  uvula, 
tonsil,  naso-pharynx,  middle  ear  and  lower  part  of  nasal  cavity.  It 
also  contains  some  taste  fibres  to  which  we  shall  refer  presently. 

The  third  or  inferior  maxillary  division  is  a  mixed  nerve.  It 
emerges  through  the  foramen  ovale.  The  motor  fibres  supply  the 
masseter,  temporal,  and  both  pterygoid  muscles,  also  the  tensor 
tympani,  mylo-hyoid  and  anterior  belly  of  the  digastric.  The 
sensory  fibres  supply  the  skin  of  the  posterior  part  of  the  temple 
and  adjacent  part  of  the  pinna,  the  anterior  and  upper  wall  of  the 
external  auditory  meatus,  as  far  as  and  including  the  anterior 
part  of  the  drum,  part  of  the  cheek,  the  lower  hp  and  chin,  also  the 
lower  teeth  and  gums,  the  tongue  (as  far  back  as  the  circumvallate 
papillse),  floor  of  mouth,  inner  surface  of  cheek,  and  saHvary  glands. 

The  Course  of  the  Taste  Fibres  is  a  compHcated  one 
and  still  much  disputed  ^  (Fig.  64).  Those  for  the  anterior  two- 
thirds  of  the  tongue  are  contained  in  the  lingual  nerve — a  branch 
of  the  third  division.  But  they  do  not  run  straight  up  from  the 
Ungual  into  the  fifth  nerve.  They  leave  the  lingual,  course  along 
the  chorda  tympani,  and  reach  the  facial  within  the  Fallopian  aque- 
duct. They  run  in  the  facial  as  far  as  the  geniculate  ganglion, 
where  some  pass  off  along  the  great  superficial  petrosal  to  Meckel's 
ganglion,  ultimately  rejoining  the  fifth  nerve  through  its  second 
division.  Other  taste  fibres  leave  the  geniculate  ganglion  to 
enter  the  nervus  intermedins,  passing  thence  to  the  glosso- 
pharyngeal nucleus. 

The  taste  fibres  for  the  posterior  third  of  the  tongue  and  the 
palate,  which  are  supplied  by  the  glosso-pharyngeal  nerve,  pro- 
bably enter  the  brain  through  the  glosso-pharyngeal.  They  do 
not  join  the  fifth  nerve,  since  division  of  the  fifth  nerve  by  the 
operation  of  removal  of  the  Gasserian  ganglion  causes  impairment 
of  taste  only  in  the  anterior  two -thirds  of  the  tongue,  and  not 
constantly  in  that.  Taste  is  not  abolished  in  fifth  nerve  palsy, 
as  was  formerly  thought,  for  in  several  cases  of  my  own  I  have 

^  Gushing,  Johns  Hopkins  Hospital  Bulletin,  1903,  Nos.  144-145.  Davioo, 
Brain,  1907,  p.  219. 


144  NERVOUS    DISEASES 

found  that  the  patient,  though  unable  to  feel  the  contact  of  food 
or  other  objects  on  one  side,  still  retained  acute  sense  of  taste  at 
the  back  of  the  tongue. 

To  examine  the  sense  of  taste  we  direct  the  patient  to  protrude 
the  tongue,  and  we  rub  on  it  various  substances  such  as  sugar,  salt, 
quinine,  and  citric  acid,  preferably  in  white  powders,  which  the 
patient  cannot  distinguish  at  sight  one  from  the  other.  The  patient 
must  keep  his  tongue  protruded   throughout  each  test,   and  as 


Fig.  65. — Paralysis  of  Left  third  and  of  Rir/ht  fifth  nerve.  The  patient  is 
looking  upwards  and  opening  the  jaw.  Showing  dilatation  of  pupil  on 
left  side  with  deficient  upward  movement  of  left  eye.  Also  showing 
the  deviation  of  the  lower  jaw  towards  the  right  side.  The  black  line 
indicates  area  of  anaesthesia  on  the  right  side  of  the  face. 

soon  as  he  feels  a  taste  he  should  make  a  sign  and  also  determine 
in  his  mind  what  the  taste  is,  before  taking  the  tongue  in.  It  is 
convenient  to  have  a  card  with  the  following  words  printed  on 
it  :_"  sweet,"  "  sour,"  "  bitter,"  "  salt,"  "  coppery."  The  patient 
can  then  point  with  his  finger  to  indicate  which  taste  he  per- 
ceives. If  he  be  allowed  to  pull  the  tongue  in  while  waiting  for 
the  sensation  to  arrive,  fallacies  may  occur  owing  to  movements 
of  the  tongue  and  the  flow  of  saliva  carrying  the  substance  to 
other  parts.  To  map  out  exactly  an  area  of  loss  of  taste  {ageusia) 
the  most  accurate  method  is  to  use  a  weak  galvanic  current  with  a 
wire  electrode,  which  produces  a  coppery  or  metallic  taste. 


CRANIAL    NERVES  145 

When  the  fifth  nerve  is  totally  ^paralysed  there  is  anaesthesia  of 
the  corresponding  half  of  the  face  and  scalp,  not  extending  as  far 
as  the  angle  of  the  jaw,  this  part  being  supplied  by  the  cervical 
plexus  (Fig.  63).  The  cornea  and  conjunctiva  on  the  aliected 
side  are  anaesthetic,  and  also  the  mucous  membrane  of  the  corre- 
sponding side  of  the  nose,  mouth,  part  of  the  soft  palate  and  tongue, 
as  far  back  as  the  circumvallate  papillae  which,  with  the  area  behind, 
are  innervated  by  the  glosso-pharyngeal.  This  defect  extends 
exactly  to  the  middle  line,  and  therefore  the  patient  when  drink- 
ing feels  as  if  the  cup  were  broken.  Food  tends  to  collect  within 
the  anaesthetic  cheek,  the  buccinator  muscle  being  anaesthetic, 
though  its  motor  power  is  unaffected.  Taste  is  impaired  in 
the  anterior  two-thirds  of  the  tongue,  but  does  not  remain  totally 
lost.  The  trigeminal  nerve  has  also  sensory  fibres  for  the  facial 
muscles.  Hence  there  is  a  degree  of  awkwardness  and  apparent 
weakness  of  the  face — a  pseudo-facial  palsy,  due  to  loss  of  the 
ssnse  of  active  muscular  contraction.  All  the  muscles  supplied 
by  the  motor  root  undergo  atrophic  paralysis  and  develop 
the  electrical  reactions  of  degeneration.  There  is  hollowing  of 
the  temporal  fossa  above  the  zygoma,  and  wasting  of  the 
masseter  below  it,  so  that  the  zygoma  becomes  abnormally 
prominent.  When  the  patient  clenches  his  teeth,  neither  the 
temporal  nor  the  masseter  can  be  felt  to  harden  as  on  the 
normal  side,  and  when  he  opens  his  mouth  the  mandible  is  pushed 
over  towards  the  paralysed  side  (Fig.  6,5).  This  is  owing  to  paralysis 
of  the  external  pterygoid,  which  fails  to  draw  the  condyle  forwards 
on  the  affected  side.  The  deflected  mandible  carries  with  it  the 
tongue,  but  there  is  no  real  deviation  of  the  tongue,  when  measured 
from  the  middle  line  of  the  lower  incisors.  It  is  stated  that  paralysis 
of  the  tensor  tympani  causes  a  difficulty  in  hearing  notes  of  low 
pitch,  but  this  is  not  easy  to  determine.  Secretion  of  tears  on  the 
paralysed  side  is  diminished,  as  is  also  the  secretion  of  nasal  mucus 
and  of  saliva.  Consequently  these  mucous  membranes  become 
abnormally  dry,  and  may  show  secondary  trophic  changes.  Thus 
stimulation  of  the  nasal  mucous  membrane  by  snufE  no  longer 
causes   sneezing.     Smell  at  first  is   unimpaired,   but  later,   from 

K 


146 


NERVOUS   DISEASES 


dryness  and  secondary  trophic  changes  in  the  Schneiderian  mem- 
brane, there  may  be  anosmia  in  the  affected  nostril.  The 
corneal  and  lachrymal  reflexes  are  lost,  also  the  palatal  reflex,  and 
the  tongue  on  the  paralysed  side  becomes  excessively  fm:red,  pro- 
bably because  on  the  anaesthetic  side  there  is  deficient  friction  by 
food.  The  teeth  on  the  paralysed  side  are  anaesthetic  and  tend  to 
drop  out ;  this  has  been  ascribed  to  a  trophic  change,  but  more 
probably  it  is  mainly  traumatic,  the  patient  biting  clumsily  with 


Fig.  66. 


Fig.  67. 


From  a  case  of  left-sided  facial  hemiatrophy.     Showing  atrophy  of 
corresponding  half  of  tongue. 


his  anaesthetic  teeth.  It  used  to  be  stated  that  neuro-paralytic  kera- 
titis occurred  in  total  trigeminal  palsy,  owing  to  trophic  changes. 
But  this  is  not  invariably  so  ;  when  it  does  occur,  it  appears  to 
be  due  to  the  presence  of  a  special  bacillus  ^  in  the  anaesthetic 
eye,  where,  moreover,  there  is  a  deficiency  of  lachrymal  secretion. 
Further,  if  the  anaesthetic  lids  be  kept  closed  by  a  suture,  keratitis 
does  not  occur,  even  though  the  special  bacillus  be  present. 

There  is  another  disease  which  occurs  in  the  territory  of  the 
^  Davies  and  Hall,  British  Medical  Journal,  1908,  p.  72. 


CRANIAL    NERVES  147 

fifth  nerve,  viz.,  progressive  facial  hemiatrophy.  This  disease,  which 
commences  in  early  Hfe — usually  before  puberty,  and  more  often 
in  females  than  in  males — shows  itself  first  in  the  skin  of  the 
face,  either  near  the  orbit  or  over  the  upper  or  lower  jaw,  gradually 
spreading  over  the  whole  face  on  one  side.  The  skin  becomes 
thinned  from  atrophy  of  its  papillary  layer,  the  subcutaneous  fat 
disappears,  and  thus  the  affected  side  of  the  face  becomes  wrinkled 
and  furrowed,  in  marked  contrast  with  the  healthy  side.  Later 
the  subjacent  muscles,  cartilages,  and  bones  become  atrophic,  but 
without  motor  paralysis  or  reaction  of  degeneration.  The  corre- 
sponding side  of  the  tongue  (Figs.  67  and  160),  and  occasionally 
that  of  the  soft  palate,  also  become  wasted.  But  the  hemi- atrophied 
tongue,  when  protruded,  comes  out  straight,  unlike  that  of  a  case 
of  atrophy  from  hypoglossal  palsy  (Fig.  81,  p.  170).  The  hair  on 
the  affected  side  of  the  face  may  fall  out  or  become  white,  and  the 
sebaceous  glands  may  atrophy.  The  scalp  is  rarely  affected.  There 
is  no  anaesthesia. 

The  area  of  this  disease  corresponds  accurately  with  that 
of  the  distribution  of  the  fifth  nerve,  and  in  certain  cases 
pathological  changes  have  been  found  either  in  the  nerve  itself  or 
in  its  nucleus  of  origin.  Thus  Mendel  found  signs  of  neuritis  in 
the  nerve,  together  with  changes  in  the  spinal  root  of  the  fifth 
within  the  medulla.  More  recently  Loebl  and  Wiesel  ^  found  an 
interstitial  neuritis  of  the  Gasserian  gangUon  and  of  the  parts 
distal  to  it.  Removal  of  the  Gasserian  ganglion  does  not  produce 
hemiatrophy.  Facial  hemiatrophy  may  also  be  a  symptom  of 
syringobulbia. 

'  Deutsche  Zeitschrijt  fiir  Nervenheilkunde,  1904,  Bd.  27,  s.  355. 


CHAPTER   X 

CRANIAL   NERVES  (continved) 

Of  all  the  peripheral  nerves  in  the  body,  cranial  or  spinal,  the 
Seventh  or  Facial  nerve  is  by  far  the  most  frequently  paralysed, 
hence  the  importance  of  knowing  its  anatomical  course  and  dis- 
tribution. Like  the  trigeminal,  it  is  a  mixed  nerve,  possessing  a 
motor  root — ^the  facial  nerve  proper,  and  a  sensory  root — the 
nervus  intermedins  of  Wrisberg.  These  two  roots  meet  at  the 
geniculate  ganglion. 

Let  us  first  consider  the  motor  root.  Arising  from  a  nucleus 
situated  mainly  in  the  lower  part  of  the  pons,  but  some  of  whose 
cells  (namely,  those  for  the  orbicularis  oculi)  extend  as  high  as 
the  nucleus  of  the  third  nerve,  and  others  (namely,  those  for  the 
orbicularis  oris)  are  as  low  as  the  hypoglossal  nucleus,  the  motor 
root  of  the  facial  pursues  a  tortuous  course.  Firstly,  within  the 
substance  of  the  pons  it  forms  a  loop  which  hooks  round  the  nucleus 
of  the  sixth  nerve.  Then,  leaving  the  ventral  surface  of  the 
brain-stem,  it  enters  the  internal  auditory  meatus,  and  passes  along" 
a  winding  bony  canal  in  the  temporal  bone — the  aqueduct  of 
Fallopius.  In  the  upper  part  of  this  canal  it  traverses  a  swelling,  the 
geniculate  ganglion,  which  is  joined  by  the  sensory  root  or  portio 
intermedia  of  Wrisberg,  also  by  the  great  superficial  petrosal  nerve 
from  Meckel's  ganglion,  and  by  the  small  superficial  petrosal  from 
the  otic  ganglion  (see  Fig.  64).  The  geniculate  ganglion  is  similar 
in  structure  to  a  posterior  root  ganglion  and  is  sensory  in  function. 
Inflammation  of  this  ganglion  is  accompanied  by  herpes  of  the 
external  auditory  canal  and  adjacent  part  of  the  auricle,  exactly 
analogous  to  herpes  zoster  ^  (see  Fig.  63,  p.  141).  Within  the 
aqueduct  the  facial  gives  off  a  branch  to  the  stapedius,  and,  lower 
down,  the  chorda  tympani  leaves  it  to  join  the  lingual  nerve.  It 
then  emerges  from  the  skull  through  the  stylo-mastoid  foramen, 

1  J.  Ramsay  Hunt,  Journal  of  Nervous  and  Mental  Diseases,  1907,  p.  73. 

14S 


CRANIAL    NERVES 


149 


giving  off  a  posterior  auricular  branch  to  the  muscles  of  the  pinna 
and  to  the  occipital  belly  of  the  occipito -frontalis.  The  main 
trunk  then  divides  into  its  terminal  branches  supplying  all  the 
muscles  of  the  face  (except  the  levator  palpebrse  superioris)  from 
the  frontalis  above  to  the  platysma  below.  It  also  supplies  the 
stylo-hyoid  and  posterior  belly  of  the  digastric. 

Although  the  facial  nerve  is  largely  motor,  the  geniculate  ganglion 
is  a  sensory  ganglion.      The  facial  also  contains  certain  secretory 


Fig.  68. 


Case  of  left-sided  facial  palsy.     Fig.  68  at  rest.     Fig.  69  on  attempt  to 
close  eyes  and  retract  angles  of  mouth. 

fibres,  whilst  the  taste-fibres  of  the  chorda  tympani  accompany  the 
motor  portion  of  the  nerve  in  part  of  its  course.  Thus  lesions  at 
different  levels  can  be  distinguished  one  from  the  other. 

1.  If  the  facial  nerve  is  affected  after  its  exit  from  the  stylo-mastoid 
foramen,  e.g.  by  cold,  or  by  injuries  or  tumours  in  that  region,  the 
result  (Bell's  Paralysis)  is  complete  palsy  of  that  side  of  the  face, 
which  is  therefore  asymmetrical  at  rest,  and  the  asymmetry  is 
exaggerated  on  voluntary  movement.  The  patient  has  neither 
emotional  nor  voluntary  movement  of  the  afiected  side  (Figs.  68 
and  69). 


150  NERVOUS    DISEASES 

Voluntary  movement  of  the  integument  by  the  platysma,  as  in 
forcible  depression  of  the  chin  against  resistance,  is  abolished  on  the^^ 

The  furrows  of  the  forehead  are  wiped  out,  and  the  patient 
cannot  wrinkle  the  brow  nor  frown  on  that  side.  The  eye  is  more 
widely  open  on  the  affected  side  and  cannot  be  shut.  The  tears 
run  down  the  cheek  instead  of  into  the  lachrymal  duct,  and  may 
produce  excoriation  of  the  skin  or  eczema.  When  the  patient 
tries  to  shut  the  eye  he  merely  rolls  the  eyeball  upwards  and 
outwards,  or  upwards  and  inwards,  sometimes  with  a  zig-zag 
movement,  until  the  cornea  passes  under  cover  of  the  upper  lid. 
An  additional  sign  pointed  out  by  Dutemps  and  Cestan  ^  is  as 
follows  : — When  the  patient  looks  down  and  then  attempts  to  shut 
both  eyes  slowly,  the  upper  lid  on  the  paralysed  side  is  seen  to 
move  up  a  little,  owing  to  contraction  of  the  levator  palpebrse, 
which  normally  acts  synergically  with  the  orbicularis  but  is  now 
no  longer  antagonised  by  it. 

This  inability  to  close  the  eye  allows  the  entrance  of  foreign 
bodies,  and  consequently  conduces  to  conjunctivitis.  The  con- 
junctival reJSex  is  abolished,  and  the  regular  involuntary  blinking 
of  health  no  longer  occurs  on  the  paralysed  side.  The  eye  brims 
over  with  tears,  so  that  vision  on  the  affected  side  is  rendered  less- 
acute.  Curiously  enough,  though  the  eye  cannot  be  shut  during 
waking  hours,  during  sleep  it  often  closes  almost  completely, 
probably  from  relaxation  of  the  levator  palpebrse. 

The  tip  of  the  nose  is  drawn  somewhat  towards  the  sound  side, 
the  naso -labial  fold  on  the  affected  side  is  flattened  out,  the  ala  nasi 
sinks  in  and  shows  no  active  movement,  voluntary  or  respiratory 
though  it  may  flap  passively  during  forcible  nasal  breathing.  The 
mouth  is  drawn  towards  the  sound  side,  but  on  the  affected  side  its 
angle  droops  and  saliva  dribbles  from  it.  When  the  patient  smiles 
or  shows  the  upper  teeth,  the  healthy  side  moves  alone  ;  he  cannot 
whistle,  and  the  articulation  of  labial  consonants  is  impaired. 
During  mastication  food  accumulates  between  the  teeth  and  the 
paralysed  cheek.  The  patient  often  bites  his  cheek  or  lower  lip,  and 
during  forcible  blowing  expiration  the  paralysed  cheek  flaps  loosely. 

1  Journal  de  Neurologic,  1904,  p.  48. 


CRANIAL    NERVES  151 

affected  side.     In  those  patients  who  were  previously  able  to  move 
the  ear  voluntarily,  that  power  is  also  lost.)  All  the  paralysed  muscles 


.v;^ 


Tears  -\ 
Taste  StSctUrcL 


Great  Saperfxxal 


Geniculate  G-an^lwrh 


/f 

/if 


■  Sweal 

•Tears  Sfy]!o7ncxsM. 

,  Toramert 

•  Taste/ SbSaZvt^a/ 


jPost^uricular 


YiQ.  70. — Diagram  of  Facial  Nerve,  showing  course  of  secretory  and  of 
taste-fibres. 


152  NERVOUS    DISEASES 

gradually  develop  the  electrical  reactions  of  degeneration.  The 
affected  side  of  the  face  generally  sweats  less  than  the  healthy  side. 
2.  If  the  lesion  be  within  the  Fallopian  aqueduct  below  the 
geniculate  gangUon,  it  produces  all  the  above  symptoms,  and,  in 
addition,  from  implication  of  the  chorda  tympani,  there  is  loss 
of  taste  (and  sometimes  slightly  of  common  sensation)  in  the 
anterior  two-thirds  of  the  tongue  on  the  affected  side,  and  also 
occasionally  abnormal  subjective  sensations  of  taste,  and  sometimes 
diminution  or  excess  of  submaxillary  and  subhngual  sahva.  The 
deficiency  of  taste  and  of  saliva  may  cause  this  part  of  the  tongue  to 
be  abnormally  furred  up  to  the  middle  line.  If  there  be  paralysis 
of  the  nerve  to  the  stapedius,  there  is  hyperacousis  or  painful 
sensitiveness  to  loud  sounds  ^  (presuming  that  the  auditory 
apparatus  is  not  affected),  and  the  patient  can  no  longer 
produce  the  subjective  noise  in  the  ear,  which  we  normally  hear 
on  attempting  very  forcibly  to  innervate  the  facial  muscles,  espe- 
cially the  orbicularis  palpebrarum. 

3.  If  the  motor  root  of  the  nerve  be  affected  between  its 
emergence  from  the  pons  and  the  geniculate  ganglion,  it  produces 
the  same  symptoms  as  in  Bell's  paralysis,  but  without  affection  of 
taste  in  the  front  of  the  tongue.  And  since  disease  in  this  region 
almost  invaiiably  implicates  the  auditory  nerve,  there  is  usually 
deafness  also.  If  the  auditory  nerve  chances  to  escape,  hyperacousis 
will  occur  from  stapedius  paralysis.  Many  cases  have  deficiency 
of  tears  on  the  affected  side.  Most  cases  of  basal  intra-cranial 
disease  present  general  symptoms  also,  such  as  headache,  giddiness 
and  vomiting. 

4.  If  the  lesion  of  the  motor  root  be  within  the  substance  of  the 
pons,  facial  palsy  results  as  in  Bell's  paralysis,  but  taste  and  hear- 
ing are  unaffected.  There  is,  however,  usually  an  accompanying 
paralysis  of  the  sixth  nerve  or  its  nucleus,  since  the  facial  motor 
root  hooks  round  the  sixth  nucleus  within  the  pons. 

Paralysis  of  the  soft  palate  used  to  be  included  in  the  symptoms  of  a 
lesion  of  the  facial  nerve  at  or  above  the  geniculate  ganglion.     But   the 

^  Moos  {Zeitschrift  fiir  Ohrenheilkunde ,  vol.  viii.  p.  221)  records  a  case  in  wliich 
the  hyperacousis  was  specially  for  low-pitched  notes. 


CRANIAL    NERVES 


153 


■\veiglit  of  evidence  goes  to  prove  that  the  facial  lias  no  share  in  the  innerva- 
tion of  the  palate.  Chvostek/  in  1883,  published  a  case  of  sarcoma  of  the 
facial  nerve  in  Avhich  paralysis  of  the  palate  had  been  observed,  but  that 
was  before  the  days  of  the  Marchi  method,  and  it  is  impossible  to  be  sure 
that  the  lower  roots  of  the  vagus  were  uudegenerated.  In  his  case  there  Avas 
also  a  cancer  in  tlie  tongue. 

Slight  cases  of  facial  palsy,  whether  due  to  cold,  middle-ear 
affection,  compression,  or  other  causes,  may  recover  completely 
in  one  or  two  weeks.     More  severe  cases  last  from  two  to  eight 


Fig.  71.  Fig.  71a. 

Case  of  left-sided  facial  palsy  with  contracture.     Fig.  71  shows  position  at  rest. 

Fig.  71a  shows  maximum  voluntary  movement. 

months  before  recovery  begins.  Or  the  palsy  may  remain  perma- 
nent. In  severe  cases,  where  improvement  does  not  begin  for 
three  months  or  more,  a  spastic  or  contracture  d  condition  usually 
comes  on  as  volun'ary  power  reappears.  The  mouth  becomes 
drawn  back  again  towards  the  paralysed  side,  the  palpebral  fissure 
instead  of  being  wider,  is  narrower  than  on  the  healthy  side,  and 
the  naso-labial  and  other  furrows  not  only  reappear,  but  become 
exaggerated.  The  result  is  that,  when  at  rest,  the  healthy  side  may 
seem  the  weaker  of  the  two,  though  when  voluntary  movement 
1  Wiener  Medizinische  Presse,  1883,  s.  34. 


154 


NERVOUS    DISEASES 


takes  place  it  is  easy  to  see  which,  is  the  affected  side  (see  Figs. 
71  and  71a).  Togelher  with  this  contracture  there  is  always 
in  the  spastic  muscles  a  tendency  to  over-action,  imperfect 
recovery  being  associated  with  imperfect  control.  One  variety  of 
facial  hemi-spasm  results  (see  p.  93).  Thus,  on  closing  the  eye 
on  the  affected  side,  the  angle  of  the  mouth  becomes  drawn  out- 
wards ;    or  again,  on  showing  the  upper  teeth,  the  eye  becomes 


FlOx.  T2. 


Fig.  72A. 


Fig.  72. — Bilateral  facial  palsy,  alcoholic  in  origin,  associated  with  peripheral 

neuritis  of  upper  and  lower  limbs. 
Fig.  72a. — Maximum  voluntary  movement  of  face,  on  attempt  to  close  the 

eyes  and  to  retract  angles  of  mouth. 

closed.  Sudden  flickers  of  involuntary  fibrillary  tremors  may 
sometimes  be  seen  on  the  affected  side.  The  spastic  facial  muscles 
can  also  be  made  to  contract  reflexly  by  tapping  lightly  over  the 
point  of  emergence  of  the  most  accessible  branch  of  the  fifth,  viz., 
the  supraorbital  nerve. ^ 

Secondary  contracture  occurs  only  in  cases  of  incomplete  re- 
covery. During  the  stage  of  total  paralysis,  when  no  impulses  are 
reaching  the  muscles,  they  are  quite  flaccid.  The  development  of 
contracture  indicates  that  muscular  regeneration  has  been  imperfect. 

^  Mondino,  Rivista  di  patologia  nervosa  e  mentale,  1907,  p.  49, 


CRANIAL    NERVES  155 

Bilateral  facial  palsy  is  rare.  It  may  be  due  either  to  intra- 
or  extra-cranial  causes,  the  commonest  intra-cranial  cause  being 
gummatous  basal  meningitis.  Of  the  extra-cranial  causes,  the 
most  important  are  double  otitis  media,  cold,  and  post-diphtheritic 
paralysis.  Alcoholic  paralysis  rarely  attacks  the  facial  nerve,  but 
when  it  does,  the  affection  is  bilateral,  as  in  the  case  of  the 
man  shown  in  Figs.  72  and  72a,  who  also  had  typical  alcoholic 
neuritis  of  the  limbs. 

In  bilateral  facial  palsy  there  is  no  asymmetry  of  the  face,  but 
it  hangs  hke  a  fixed  expressionless  mask,  incapable  of  evincing 
the  slightest  emotion. 

Bilateral  facial  weakness  also  occurs  in  the  "  facio-scapulo- 
humeral "  type  of  myopathy,  to  which  we  shall  refer  in  a  later 
chapter. 

Nervus  Intermedius  of  Wrisberg-,  or  Sensory  Root  of  the 
Facial. — Between  the  facial  motor  root  and  the  auditory  nerve  at 
the  floor  of  the  cranial  cavity,  and  entering  the  internal  auditory 
meatus  along  with  them,  there  is  a  slender  fasciculus,  known  as  the 
fortio  intermedia.  The  fibres  of  this  nerve  are  remarkably  small 
in  calibre.  Their  trophic  centre  is  in  the  cells  of  the  geniculate 
ganglion.  Centrally  the  fibres  run  into  the  bulb,  alongside  the 
fibres  of  the  auditory  nerve,  to  join  a  nucleus  closely  connected 
with  that  of  the  glosso-pharyngeal.  Peripherally  from  the 
geniculate  gangUon  fibres  run  along  the  great  and  small  super- 
ficial petrosal  nerves  ;  others  along  the  trunk  of  the  facial,  in 
the  chorda  tympani.  The  nervus  intermedius  probably  conveys 
taste  impulses  upwards  to  the  brain,  by  way  of  the  glosso- 
pharyngeal nucleus  (Fig.  70,  p.  151).  And  it  appears  to  contain 
also  efferent  fibres  which  join  the  submaxillary  ganglion.  Inflam- 
mation of  the  geniculate  ganglion,  analogous  to  inflammation  of 
the  posterior  root  ganglion  in  herpes  zoster,  as  Hunt  has 
pointed  out,  produces  characteristic  symptoms.  These  consist 
in  pain  and  herpes  of  the  auricle  and  external  auditory  canal. 
If  the  inflammation  be  intense  enough  to  implicate  the  motor 
fibres  of  the  facial  there  is  facial  palsy  also,  with  loss  of  taste  in 
the    chorda    tympani   distribution.       If    the    auditory    nerve    be 


156  NERVOUS    DISEASES 

implicated  there  is  vertigo,  tinnitus,  deafness  and  even  nausea 
and  vomiting. 

The  Eighth  or  Auditory  Nerve  comprises  two  entirely 
different  sets  of  fibres.  (See  Fig.  24,  p.  40.)  Firstly,  there  are 
cochlear  fibres  for  the  function  of  hearing.  Secondly,  there  are 
vestibular  fibres  which  supply  the  semicircular  canals  and  constitute 
the  most  important  nerve  of  equilibration,  informing  us  of  the  posi- 
tion of  our  head  in  space.  Affections  of  the  cochlear  fibres  produce 
one  form  phenomena,  while  disease  of  the  vestibular  fibres  causes 
auditory  of  vertigo,  though  vertigo  and  other  auditory  symptoms 
often  result  not  only  from  disease  of  the  labyrinth  or  vestibular 
fibres,  but  from  affections  of  the  middle  or  even  of  the  outer  ear. 

The  chief  symptoms  referable  to  the  auditory  nerve  are  deaf- 
ness, tinnitus  and  vertigo. 

In  a  patient  who  is  apparently  deaf  we  should  always,  before 
proceeding  to  test  the  hearing,  examine  the  external  auditory 
meatus,  to  make  sure  that  it  is  not  blocked,  e.g.  by  wax.  We 
then  test  aerial  conduction  by  the  ticking  of  a  watch,  the 
patient's  eyes  being  shut  and  one  ear  closed  while  the  other 
is  being  tested.  Holding  the  watch  at  some  distance  from 
the  ear,  we  slowly  bring  it  nearer  until  the  patient  can  just  detect 
the  tick.  If  there  is  deafness,  we  have  to  determine  whether 
this  is  due  to  middle- ear  disease  or  to  affection  of  the  labyrinth 
or  auditory  nerve.  The  tuning-fork  tests  help  us  here.  Normally 
a  vibrating  tuning-fork,  preferably  C^  ( =  256  vibrations  per  second) 
placed  on  the  vertex  or  centre  of  the  forehead  is  heard  equally  in 
both  ears  (Weber's  test),  and  if  one  ear  be  temporarily  closed  by 
the  finger,  the  note  is  heard  louder  on  that  side.  If  the  tuning- 
fork  be  placed  on  the  mastoid  process,  we  wait  till  it  is 
no  longer  heard  through  the  bone,  and  find  normally  that  it 
is  still  audible  when  held  close  to  the  external  meatus  (Rinne's 
test).  If  the  middle  ear  be  diseased,  or  if  the  outer  ear  be  blocked 
up,  there  is  loss  of  aerial  conduction,  but  bone-conduction  is  still 
preserved.  The  tuning-fork  on  the  vertex  is  then  heard  louder  on 
the  affected  side  ("  positive -Weber,")  and  Rinne's  test  is  negative, 
i.e.  the  tuning-fork  is  no  longer  heard  aerially  after  fading  away  on 


CRANIAL   NERVES  157 

bone-conduction.  But  if  the  deafness  be  due  to  affection  of  the 
internal  ear  or  of  the  auditory  nerve — so-called  "  nerve-deafness," 
a  tuning-fork  on  the  vertex  is  not  heard  on  the  affected  side 
("negative-Weber"),  whilst  as  a  rule  there  is  "  positive-Rinne," 
though  not  always.  In  deafness  from  chronic  middle-ear  catarrh, 
the  hearing  is  generally  better  in  the  midst  of  a  noise  {e.g.  in  an 
omnibus  or  railway  carriage),  than  in  a  quiet  place  : — so  called  ^ar- 
«cowsw, %hereas  in  nerve -deafness  the  reverse  is  the  case.  Additional 
localising  evidence  may  also  be  obtained  from  the  other  concomitant 
symptoms.  Thus  gross  disease  of  the  auditory  nerve  within  the 
skull,  e.g.  in  a  case  of  lateral  extra -cerebellar  tumour,  is  often 
accompanied  by  facial  paralysis,  though  this  conjunction  is  of 
value  only  when  middle-ear  disease  can  be  excluded.  On  the 
other  hand,  disease  of  the  labyrinth  is  often  associated  with  tinnitus 
or  vertigo,  and  labyrinthine  deafness  is  specially  characterised  by 
loss  of  perception  for  high-pitched  tones,  as  tested  by  Galton's 
whistle.  Disease  of  the  auditory  nuclei  within  the  pons  may  be 
associated  with  weakness  of  the  motor  facial  nerve  of  the  same 
side  and  paralysis  of  the  opposite  arm  and  leg. 

Tinnitus,  or  ringing  in  the  ears,  is  a  subjective  symptom.  It 
signifies  irritation  of  some  part  of  the  auditory  apparatus.  The 
term  does  not  include  elaborate  auditory  hallucinations  of  cortical 
origin,  such  as  distinct  melodies  or  voices  uttering  intelligible 
words.  The  nature  of  the  sound  in  tinnitus  varies  in  different 
cases ;  for  example,  it  may  be  buzzing,  hissing  or  whistling. 
Broadly  speaking,  we  recognise  two  main  kinds  of  tinnitus — the 
pulsating  and  the  continuous.  Pulsating  sounds,  synchronous  with 
the  pulse,  occur  in  a  few  intra-cranial  aneurisms  (sometimes 
audible  by  the  physician  on  auscultation  of  the  skull),  but  are  also 
not  infrequent  in  simple  neurasthenia  in  the  "  silent  watches  of  the 
night,"  and  in  temporary  Eustachian  obstruction,  as  in  some  cases 
of  coryza.     Curious  "  clicking  "  sounds  in  the  ear  may  result  from 

^  Paracousis,  according  to  some  observers,  is  associated  with  abnormally  low 
labyrinthine  pressure,  and  the  temporary  improvement  of  hearing  in  such 
patients  during  a  noisy  journey,  in  a  railway  carriage  or  motor  car,  is  due  to  a 
reflex  contraction  of  the  stapedius  muscle  pushing  inwards  the  foot  of  the  stapes 
and  raising,  for  the  time  being,  the  pressure  of  the  endolymph  (see  A.  Cheatle, 
Trans.  Otol.  Soc,  1900,  vol.  i.  p.  52  ;  also  C.  Heath). 


158  NERVOUS   DISEASES 

clonic  spasm  of  the  tensor  tympani  muscle.  Continuous  sounds 
may  be  of  high  or  low  pitch.  We  should  always  notice  whether 
they  are  increased  or  diminished  by  the  recumbent  posture.  Low- 
pitched  continuous  tinnitus  may  be  the  result  of  venous 
hypereemia,  in  which  case  it  is  aggravated  by  recumbency,  or 
of  simple  anaemia,  which  is  relieved  by  lying  down.  Nitrite 
of  amyl  aggravates  tinnitus  when  due  to  hypersemia  and  relieves 
it  when  due  to  ansemia.  High-pitched  continuous  tinnitus  is 
generally  due  to  labyrinthine  stimulation,  either  from  outer  or 
middle- ear  affection  (perhaps  merely  wax  or  water  in  the  external 
meatus,  an  obstructed  Eustachian  tube,  or  an  indrawn  tympanic 
membrane),  or  from  actual  labyrinthine  disease.  It  is  also  caused 
by  certain  drugs,  notably  by  quinine  and  salicylates.  Such  drugs 
induce  deafness  as  well  as  tinnitus,  and  the  tinnitus  may  persist 
for  weeks  after  the  deafness  has  cleared  up.  Pulsating  tinnitus 
due  to  arterial  congestion  can  often  be  arrested  temporarily  by 
compression  of  the  vertebral  artery  supplying  the  labyrinth,  or  of 
the  carotid  supplying  the  external  or  middle  ear.-^ 

Vertigo,  or  giddiness,  is  the  pecuhar  disagreeable  sensation 
which  results  if  our  sense  of  secure  equilibration  is  disturbed.  The 
process  of  equilibration  is  a  muscular  act,  where  all  the  muscles  are 
innervated,  of  course,  by  the  cerebral  cortex,  this  latter  being  again 
largely  influenced  by  the  cerebellum.  The  cerebellum  is  a  co- 
ordinating centre  for  equihbration.  It  receives  afferent  impulses 
from  various  sources,  of  which  the  semicircular  canals  of  the  inner 
ear  are  by  far  the  most  important,  the  others  coming  from  the  skin 
of  those  parts  on  which  the  body  happens  to  be  resting,  from  the 
muscles  and  joints  concerned  in  maintaining  our  balance,  and  from 
the  muscles  of  the  head  and  eyes  concerned  in  looking  towards  sur- 
rounding objects.  Each  half  of  the  cerebellum  exercises  a  co- 
ordinating influence,  through  the  corresponding  superior  cerebellar 
peduncle,  upon  the  contra-lateral  cerebral  cortex,  and  thus  upon 
the  muscles  of  the  ipso-lateral  hmbs. 

Giddiness  is  often  accompanied  by  a  feeling  of  movement 
either  in  the  patient  himself  (subjective  vertigo)   or  in  external 

1  Dundas  Grant,  Brit.  Med.  Journal,  Dec.  24,  1887. 


CRANIAL    NERVES  159 

objects  (objective  vertigo).  Severe  giddiness  usually  produces  the 
motor  phenomenon  of  reeling  or  staggering. 

Vertigo  may  result  from  affection  either  of  the  higher  cerebral 
centres  or  of  the  co-ordinating  cerebellar  centres,  or  from  affection 
of  any  of  the  afferent  paths  to  which  we  have  already  referred. 
Severe  vertigo  is  often  accompanied  by  nausea  and  vomiting,  as  in 
sea -sickness. 

Vertigo  may  occur  in  healthy  people.  Thus,  for  example,  a 
galvanic  current  of  10  to  15  milliamperes  passed  transversely 
through  the  head  produces  a  variety  of  giddiness  probably  due  to 
labyrinthine  stimulation.  In  this  the  patient  tends  to  fall  to- 
wards the  side  of  the  positive  pole,  and  his  head  and  eyes  are  also 
rotated  in  that  direction,  accompanied  by  a  rotatory  nystagmus, 
until  the  moment  of  stopping  the  current,  when  he  tends  to  fall  to- 
wards the  side  of  the  negative  pole.  Rapid  rotation  of  the  body 
round  its  own  axis,  as  in  waltzing,  or  rapid  changes  in  our  position 
in  space,  as  in  swinging,  produce  giddiness  which  is  probably  due  to 
variations  in  the  pressure  of  the  endolymph  within  the  semicircular 
canals.  Some  people  feel  giddy  when  stepping  unexpectedly  from 
a  firm  surface  on  to  a  piece  of  boggy  turf,  or,  as  in  a  famous 
Edinburgh  street,  on  to  a  piece  of  indiarubber  pavement,  this 
variety  of  vertigo  being  due  to  deficient  sense  of  resistance  con- 
veyed from  the  skin  of  the  soles  and  from  the  muscles  and  joints 
of  the  lower  limbs.  The  giddiness  produced  by  standing  near  the 
edge  of  a  cliff  or  of  a  high  tower  is  most  probably  due  to  loss  of 
muscular  impression  from  the  ocular  muscles.  Ordinarily  we  have 
surrounding  objects  at  or  above  our  own  level  with  which  to 
compare  our  position  in  space,  and  if  such  objects  are  absent 
vertigo  may  result. 

Vertigo  is  also  associated  with  various  pathological  conditions. 
Among  the  intra-cranial  causes  we  may  mention  blows  on  the 
head  (this  variety  is  often  relieved  by  repeated  small  doses,  about 
-Jy  grain,  of  perchloride  of  mercury),^  and  sudden  cerebral  ancemia  or 
hypercemia.  A  distinguished  member  of  the  medical  profession 
who  was  the  subject  of  aortic  regurgitation  used  to  have  attacks  of 

^  Dundas  Grant,  Clinical  Journal,  Oct.  9,  1907. 


160  NERVOUS    DISEASES 

intense  vertigo  if  he  took  a  saline  aperient.  Probably  in  his  case 
the  withdrawal  of  a  considerable  amount  of  fluid  from  the  circula- 
tion rendered  the  brain  anaemic — ^hence  the  vertigo.  It  was  always 
relieved  by  the  recumbent  posture,  while  cardiac  tonics  and  the 
avoidance  of  hydragogue  cathartics  prevented  its  recurrence. 
Vertigo  from  cerebral  hypersemia  is  very  common  in  women  about 
the  menopause,  also  in  the  arterio -sclerosis  of  chronic  renal  disease. 
In  the  latter  class,  relief  is  often  obtained  by  the  administration  of 
iodides.  It  is  still  more  marked  in  many  cases  of  cerebral  haemor- 
rhage or  thrombosis,  of  which  it  may  be  a  premonitory  signal. 
Giddiness  in  old  people  with  atheromatous  arteries,  if  it  be 
associated  with  headache,  and  especially  if  there  be  no  sign  of 
labyrinthine  disease,  should  always  be  regarded  with  caution. 
Intra-cranial  tumours  may  cause  giddiness  by  raising  the  general 
pressure  within  the  skull,  and  cerebellar  tumours  are  especially 
associated  with  vertigo,  even  apart  from  increased  intra-cranial 
pressure.  Intra-cerebellar  tumours  of  the  lateral  lobe  produce  a 
vertigo  in  which  the  subjective  sense  of  rotation  of  the  body  is  in 
the  same  direction  as  that  of  the  apparent  movement  of  surrounding 
objects,  i.e.  away  from  the  side  of  the  lesion.  In  extra-cerebellar 
tumours,  while  external  objects  appear  to  move  away  from  the 
side  of  the  lesion,  the  sense  of  subjective  rotation  is  reversed,  i.e. 
towards  the  side  of  the  lesion. 

A  characteristic  form  of  vertigo  has  also  been  described  by 
Bruns,^  and  confirmed  by  various  other  observers.^  It  is  pro- 
duced by  the  presence  of  a  cysticercus  in  the  fourth  ventricle. 
Sometimes  the  worm  is  anchored  to  the  ependyma,  sometimes  it 
is  swimming  free.  The  patient,  who  otherwise  shows  no  sign  of 
intra-cranial  organic  disease,  has  paroxysms  of  violent  vertigo, 
chiefly  on  sudden  movement  of  the  head,  either  active  or  pas- 
sive, causing  a  temporary  shifting  of  the  position  of  the  worm. 
He  also  has  attacks  of  occipito-frontal  headache  with  vomiting  ; 
his  gait  is  tottering  and  unsteady,  and  glycosuria  is  not  uncom- 
monly present.     There  may  be  intervals  during  which  he  is  ap- 

1  Centralblatt  fur  Neurologic,  1902,  s.  565. 
2  Osterwald,  Neurologisches  Centralhlatt,  1906,  s.  265. 


CRANIAL  NERVES  161 

parently  well,  and  the  case  may  be  mistaken  for  hysteria.  Death 
usually  occurs  suddenly  from  respiratory  paralysis. 

Vertigo  is  associated  with  certain  degenerative  diseases,  notably 
with  disseminated  sclerosis.  Vertigo  is  frequently  the  "aura" 
of  an  epileptic  fit,  or  may  accompany  the  headache  of  an  attack 
of  migraine.  A  hereditary  family  form  of  giddiness  has  also 
been  described. 

Toxic  vertigo  from  alcohol  or  tobacco  is  a  familiar  type,  and 
to  the  toxic  class  we  may  also  refer  cases  produced  by  gastric 
disorder,  by  constipation,  and  by  some  cases  of  intestinal  parasites, 
though  in  the  last  instance  a  reflex  element  may  also  be  present. 
Giddiness  is  often  present  in  neurasthenic  and  hysterical  patients, 
in  whom  it  may  be  elicited  by  the  slightest  exciting  cause,  for 
example  by  rectal  examination. 

Ocular  vertigo  occurs  in  cases  of  paralysis  of  any  of  the  external 
ocular  muscles,  and  is  associated  with  diplopia.  The  visual  field 
being  erroneously  projected,  the  patient  judges  wrongly  as  to 
the  relation  of  his  body  to  what  he  sees.  "  Objects  appear  to  be 
in  certain  positions  where  the  patient's  feet,  as  a  matter  of  fact, 
fail  to  find  them  "  (Hughlings  Jackson).  The  giddiness  in  such 
cases  is  not  due  directly  to  the  diplopia,  for  it  persists  when  the 
sound  eye  is  covered.  The  condition  can  be  imitated  in  health  by 
closing  one  eye  and  displacing  the  other  eye  inwards  by  pressure 
with  the  finger,  when  if  the  subject  tries  to  walk  along  a  straight 
line  his  gait  becomes  very  unsteady. 

But  in  the  vast  majority  of  cases  vertigo  is  associated  with 
some  disorder  of  the  ear.  It  may  result  from  wax,  or  foreign  bodies 
in  the  meatus,  or  it  may  supervene  during  ear-syringing,  especially 
if  there  is  a  perforation  of  the  drum.  The  pathological  cause  may 
also  be  in  the  middle  ear,  as  in  otitis  media  or  obstruction  of  the 
Eustachian  tube,  or  the  condition  may  result  merely  from  sneezing 
or  blowing  the  nose,  also  from  spasm  of  the  tensor  tympani  muscle. 

Lastly,  there  is  what  is  known  as  Meniere's  disease,  or  laby- 
rinthine vertigo.  This  has  three  main  classes  of  symptoms : 
firstly,  giddiness  and  reehng,  due  to  affection  of  the  semicircular 
canals  ;  secondly,  deafness   and   tinnitus,  due  to  affection  of  the 


162  NERVOUS    DISEASES 

auditory  fibres  ;  and  thirdly,  associated  bulbar  phenomena,  such,  as 
nausea  and  vomiting,  cardiac  failure,  cold  clammy  sweat,  &c.,  due 
to  affection  of  adjacent  medullary  centres. 

The  vertigo  of  Meniere's  disease  is  paroxysmal,  and  comes  on 
with  such  suddenness  that  the  patient  may  fall  to  the  ground  as 
if  struck  down  by  an  unseen  hand.  In  other  cases  he  reels,  but 
has  time  to  clutch  at  some  neighbouring  object  to  prevent  him- 
self from  falhng.  The  giddiness  lasts  sometimes  for  hours ; 
shghter  attacks  may  pass  off  in  a  few  minutes.  It  is  increased 
by  movement,  and  the  slightest  attempt  to  raise  the  head  may 
induce  vomiting.  The  direction  in  which  the  patient  falls  is 
usually  forwards  or  towards  one  side,  and  commonly  away  from 
the  side  of  the  affected  ear.  Not  infrequently  nystagmoid  jerks 
of  the  eyes  occur  during  the  attack,  and  double  vision  has  also 
been  observed.  The  vertigo  is  frequently  accompanied  or  followed 
by  headache,  nausea  and  vomiting,  lasting  sometimes  for  hours. 
Together  with  these  there  are  characteristic  auditory  phenomena, 
generally  a  sudden  loud  noise,  usually  unilateral.  There  is  also 
deafness,  more  or  less  complete,  on  the  same  side  as  the  tinnitus, 
with  diminution  or  loss  of  bone-conduction.  A  certain  degree  of 
deafness  remains  between  the  attacks,  but  is  rarely  absolute. 

Such  symptoms,  occurring  with  apoplectiform  suddenness, 
constitute  the  typical  picture  of  Meniere's  disease.  But  frequently 
ths  paroxysms  are  much  slighter,  and  unassociated  with  nausea 
or  vomiting,  so  that  the  patient  may  simply  have  sudden  transient 
giddiness.  But  the  attacks  tend  to  recur  ;  rarely  does  a  patient 
escape  with  a  single  attack.  The  intervals  between  them  vary ; 
they  may  gradually  decrease  in  frequency,  or  may  progressively 
increase  until  after  successive  attacks  the  deafness  becomes 
absolute.     The  vertigo  then  usually  ceases. 

Meniere's  disease  is  distinguished  from  epileptic  vertigo  by  the 
coexistence  of  vertigo  with  tinnitus  and  deafness.  Loss  of  con- 
sciousness, which  is  the  rule  in  epilepsy,  is  rare  in  labyrinthine 
vertigo.  Labjo-inthine  vertigo  often  yields  to  small  doses  (|  to  1 
grain)  of  quinine.  From  cerebral  haemorrhage  or  thrombosis  it  is 
distinguished  by  the  presence  of  auditory  phenomena,  and  by  the 


CEANIAL   NERVES  163 

absence  of  signs  of  a  focal  brain  lesion.  The  pathology  of  Meniere's 
syndrome  is  obscure.  Meniere  himself  described  a  heemorrhagic 
effusion  in  the  inner  ear.  But  as  Arthur  Cheatle  ^  has  lumin- 
ously suggested,  the  phenomena  are  in  many  respects  closely 
analogous  to  those  of  glaucoma,  and  may  possibly  be  due  to  a 
sudden  rise  of  tension  in  the  endolymph  or  perilymph,  whether 
produced  by  haemorrhage  or  other  causes  in  the  labyrinth  or  by 
sclerosis  of  the  middle  ear,  whereby  the  fenestra  ovalis  and  fenestra 
rotunda  become  fixed,  thereby  depriving  the  inner  ear  of  safety- 
valves  which  normally  permit  of  compensation  for  sudden  changes 
in  labyrinthine  pressure. 

A  focal  lesion  of  Deiters'  nucleus  (as  has  been  shown  by 
Bruce  and  by  Bonnier)  produces  sudden  vertigo  and  reehng, 
together  with  nausea,  acute  distress,  transient  tinnitus  or  deaf- 
ness, nystagmus,  and  sometimes  pain  in  the  distribution  of  the 
trigeminal  nerve.  All  these  phenomena  are  easily  exphcable 
when  we  remember  the  connection  of  Deiters'  nucleus  with  the 
cerebellum  and  with  the  oculomotor  nerves,  and  its  close 
proximity  to  the  sensory  nucleus  of  the  trigeminal. 

No  case  of  isolated  palsy  of  the  Ninth  or  Glosso-pharyngeal 
Nerve  has  yet  been  observed  in  man,  so  that  its  exact 
functions  are  not  completely  determined.  We  know  that  it  sup- 
plies taste -fibres  to  the  posterior  third  of  the  tongue  and  to  the 
soft  palate.  It  probably  also  suppHes  the  taste  buds  which  exist 
on  the  epiglottis  and  on  the  arytenoid  cartilage.  The  glosso- 
pharyngeal is  also  a  nerve  of  common  sensation  for  the  back  of  the 
tongue,  part  of  the  soft  palate  and  upper  part  of  the  pharynx, 
whilst  it  has  motor  fibres  for  the  middle  constrictor  of  the  pharynx, 
and  for  the  stylopharyngeus. 

Paralysis  of  the  nerve  causes  anaesthesia  of  the  back  of  the 
tongue  and  pharynx,  difficulty  in  swallowing  and  deficient  taste 
in  the  posterior  third  of  the  tongue.  In  animals  where  this  nerve 
has  been  divided  experimentally,  the  pharynx  and  oesophagus 
remain  tonically  contracted,  owing  to  paralysis  of  the  inhibitory 
fibres  contained  in  the  glosso-pharyngeal. 

1  Archives  of  Otology,  vol.  xxvi.,  1897,  p-  185. 


164 


NERVOUS    DISEASES 


The  Tenth  Nerve,  Vagus,  or  Pneumogastric  Nerve,  according 
to  modern  nomenclature,  is  held  to  include  those  roots  which  used 
to  be  called  the  "  bulbar  part  of  the  spinal  accessory."  Nowadays 
the  term  "  spinal  accessory  "  is  limited  to  the  spinal  part  of  the 
accessorius  which  arises  from  an  entirely  separate  nucleus,  where- 
as the  old  "  bulbar  part "  is  derived  from,  and  belongs  to,  a 
continuation  of  the  vagus  nucleus  (nucleus  ambiguus)  in  the 
medulla. 

The  vagus  has  a  most  extensive  distribution.  It  supphes  the 
pharynx,  larynx,  oesophagus,  heart,  lungs,  stomach,  and  partly 
even  the  intestines  and  spleen.     By  its  auricular  branch  it  also 


Fig.  73. — Paralysis  of  the  right  side  of  the  palate.  The  patient  is  saying 
"  Ah,"  and  the  palate  is  pulled  up  towards  the  left  side.  The  arrow 
points  to  the  centre  of  the  uvula. 

supplies  part  of  the  skin  of  the  outer  ear.  Its  pulmonary  fibres 
are  motor  for  the  bronchial  muscles  and  sensory  for  the  respiratory 
passages.  The  vagus  is  both  motor  and  sensory  for  the  oesophagus, 
sensory  for  the  stomach,  and  partly  motor  for  the  stomach  and 
intestines.  Its  lowest  roots  of  origin  are  those  which  are  of  the 
greatest  diagnostic  importance,  for  they  contain  motor  fibres 
for  the  levator  palati  and  the  larynx,  together  with  inhibitory 
fibres  for  the  heart.  With  the  exception  of  the  crico-thyroid 
muscle,  which  is  innervated  by  the  superior  laryngeal  branch, 
all  the  laryngeal  muscles  are  supplied  through  the  inferior  or 
recurrent  laryngeal  nerve. 

The  symptoms  of  vagus  paralysis  vary  according  to  the  site 
of  the  lesion.  Intra-cranial  lesions  may  affect  all  its  roots  of  origin, 
or  may  attack  the  upper  or  the  lower  roots  alone.     In  the  latter 


CRANIAL   NERVES 


165 


case    there    is    often    a    concomitant    affection    of    the    adjacent 
hypoglossal  nerve. 

If  the  whole  of  one  vagus  trunk  be  aflected,  there  is  unilateral 
paralysis  of  the  palate  and  larynx  (Avellis's  syndrome),  together 
with  anaesthesia  of  the  larynx  on  the  affected  side.  The  only  way 
to  recognise  a  unilateral  paralysis  of  the  palate  is  to  watch  the 
movement  of  its  median  raphe  when  the  patient  utters  a  long 


Fig.  74. — Organic  laryngeal  paralyses  (Barwell). 

I.  Left  abductor  paralysis,  during  inspiration. 
II.  Left  abductor  paralysis,  during  phonation. 

III.  Left  recurrent  laryngeal  paralysis,  during  inspiration. 

IV.  Left  recurrent  laryngeal  paralysis,  during  phonation. 

"  Ah."  Normally  the  raphe  rises  straight  up.  But  if  one  side  of 
the  palate  be  paralysed,  the  healthy  side  alone  pulls  upwards  and 
the  raphe  deviates  to  the  sound  side,  forming  a  characteristic 
dimple  (Fig.  73). 

If  both  vagi  be  paralysed,  there  is  tachycardia  and  irregularity 
of  the  heart,  from  paralysis  of  the  cardio-inhibitory  fibres.  There 
are  also  slowness  and  irregularity  of  respiration.  These  do  not 
occur  in  unilateral  vagus  palsy.  Gastric  symptoms  have  also 
been  observed  even  in  unilateral  cases,  such  as  gastric  dilatation. 


166 


NERVOUS    DISEASES 


vomiting,   gastric  pain,   and  loss  of  the  sensations  of  hunger  and 
thirst. 

Of  all  these  symptoms,  the  most  constant  and  easiest  to 
recognise  are  the  afiection  of  the  soft  palate  and  the  laryngeal 
palsy.  Paralysis  of  the  recurrent  laryngeal  nerve  may  occur 
alone.  The  commonest  cause  is  aortic  aneurism,  which  frequently 
compresses    the    nerve    on   the    left    side.      Mediastinal   growths 


Fig.  75.— Functional  laryngeal  paralyses  (Barwell). 

V.  Adductor  paresis — all  the  adductors  affected — phonation. 
VI.  Adductor  paresis — arytenoideus  unaffected — phonation. 
VII.  Paralysis  of  the  thyro-arytenoidei — phonation. 
VIII.  Paralysis  of  the  arytenoideus — phonation. 

may  also  compress  it,  or  its  paralysis  may  even  be  the  result 
of  mitral  stenosis,  where  the  left  auricle  becomes  dilated  and  thus 
compresses  the  nerve  directly  against  the  pulmonary  artery,  or  the 
auricle  may  force  the  left  bronchus  upwards  and  compress  the  nerve 
against  the  aortic  arch.^  In  recurrent  laryngeal  paralysis  the  vocal 
cord  on  the  affected  side  is  immobile,  fixed  in  the  cadaveric 
position,  i.e.  midway  between  abduction  and  adduction,  and  the 
voice  is  generally  hoarse  though  not  absent,  since  during  phonation 
the  healthy  cord  can  cross  the  middle  line  to  meet  the  paralysed 
1  Frischauer,  Wiener  Klin.  Wochenschrift,  Dec.  28,  1905. 


CRANIAL    NERVES 


167 


one.  If  both  recurrent  laryngeah  be  paralysed,  both  vocal  cords  are 
motionless  and  in  the  cadaveric  position,  and  phonation  is  impossible 
since  the  cords  cannot  be  brought  together.  There  is  no  stridor 
except  on  deep  inspiration. 

It  is  here  convenient  to  recall  some    of  the  chief  diagnostic 
features  of  laryngeal  palsies  (Figs.  74  and  75).     Abductor  palsy, 


Fig.  76. 


Fig. 


Paralysis  of  right  spinal  accessory  nerve. 

Fig.  76  shows  the  downward  and  outward  disialacement  of  the  right  scapula.  Observe 
alteration  in  the  lateral  outlines  of  the  neck.  On  the  paralysed  side  the  outline  is 
formed  by  the  levator  anguli  scapulre  ;  on  the  normal  side  by  the  trapezius. 

Fig.  77  shows  the  patient  attempting  to  depress  the  head  against  resistance.  Observe  the 
absence  of  the  right  sterno-mastoid,  the  right  omo-hyoid  being  now  subcutaneous. 


unilateral  or  bilateral,  is  always  organic,  and  is  often  the  earhest 
sign  of  a  commencing  recurrent  laryngeal  nerve  affection.  In  uni- 
lateral ahductor  palsy  the  voice  is  unaffected,  but  on  laryngoscopic 
examination  the  paralysed  cord  is  seen  to  be  immobile  during 
inspiration,  not  moving  outwards  Uke  its  healthy  fellow.  On 
phonation  the  cords  meet  normally.  In  bilateral  abductor  palsy 
the  voice  is  also  unaffected,  since  both  cords  come  together  on 
phonation.  And  since  they  no  longer  move  outwards  during  in- 
spiration, but  on  the  contrary  are  sucked  together,  inspiration  is 
laboured  and  stridulous,  and  the  patient  is  in  danger,  since  the 


168  NERVOUS    DISEASES 

slightest  swelling  of  the  cords  may  completely  block  the  glottis. 
Paralysis  of  the  internal  thyro-arytenoid  muscle,  which  occurs  in 
some  cases  of  early  bulbar  paralysis,  is  characterised  by  an  oval 
instead  of  a  linear  appearance  of  the  glottis  on  attempted  phona- 
tion,  owing  to  loss  of  the  support  of  these  muscles.  The  voice  is 
therefore  hoarse,  but  abduction  and  adduction  are  otherwise 
unafEected.     Adductor  paralysis  is  always  bilateral  and  generally 


Fi6.  78. — Paralysis  of  right  spinal  accessory  nerve,  showing  downward 
and  outward  displacement  of  scapula.  Owing  to  absence  of 
the  trapezius,  the  rhomboid  muscles  on  the  right  side  have  become 
subcutaneous. 

hysterical.  It  is  common  in  hysterical  aphonia.  The  patient 
loses  her  voice,  often  suddenly,  and  talks  in  a  whisper.  There 
is  no  stridor,  and  on  inspiration  the  cords  move  normally  out- 
wards. But  on  attempted  phonation  they  do  not  reach  the 
middle  line.  The  condition  often  disappears  suddenly,  sometimes 
as  a  result  of  the  process  of  laryngoscopy,  or  of  the  application 
of  strong  faradic  shocks  to  the  lar3nix. 

The  Eleventh  or  Spinal  Accessory  Nerve  is  distributed  to  the 
sterno-mastoid  and  to  part  of  the  trapezius.  It  is  exclusively  a 
motor  nerve.  When  it  is  paralysed,  we  have  paralysis  and  atrophy 
of  the  sterno-mastoid,  which  no  longer  stands  out  on  rotation  of 


CRANIAL    NERVES 


169 


the  head  to  the  opposite  shoulder,  nor  on  depressing  the  head  against 
resistance  (Figs.  76  and  77).  The  paralysis  of  the  trapezius  varies 
in  degree  according  to  the  extent  to  which  the  muscle  is  supplied 
by  the  spinal  accessory  and  by  the  cervical  plexus  respectively. 
Ordinarily  the  uppermost  fibres  of  the  trapezius  are  innervated  by 
the  spinal  accessory,  whilst  the  middle  fibres  of  the  muscle  are  sup  - 
plied  by  the  third  and  fourth  cervical  nerves,  and  the  lowest  fibres 


Fig.  79.  i'lG.  80. 

Paralysis  of  right  spinal  accessory  nerve. 
Fig.  79. — Showing  position  at  rest. 
Fig.  80. — Showing  position  on  adduction  of  scapula;. 

of  all  by  the  spinal  accessory.  When  the  trapezius  is  paralysed, 
the  outline  of  the  neck  is  altered,  owing  to  the  levator  anguU 
scapulae  having  become  subcutaneous,  and  there  is  a  characteristic 
deformity  of  the  angle  of  the  shoulder  resulting  from  the  displace- 
ment of  the  scapula  (Fig.  78).  The  scapula  on  the  paralysed  side 
is  displaced  downwards  and  outwards,  and  rotated  outwards,  so 
that  its  inner  border  instead  of  being  parallel  with  the  spine,  is 
inclined  from  below  upwards  and  outwards.  When  the  patient 
braces  his  shoulders  back,  the  scapula  i?  imperfectly  approximated 
to  the  middle  line,  and  the  rhomboids  on  the  paralysed  side  are 
visible  subcutaneously  (Figs.  79  and  80). 


170  NERVOUS    DISEASES 

The  Twelfth  or  Hypoglossal  Nerve  is  also  entirely  motor  in 
function.  Immediately  after  its  exit  from  the  skull  it  receives 
amongst  other  connections  a  small  communicating  branch  from  the 
cervical  sympathetic.  The  hypoglossal  supplies  all  the  intrinsic 
muscles  of  the  corresponding  half  of  the  tongue.     Outside  the  skull 


Fig.  81. — Paralysis  of  right  hypoglossal  nerve  from  a  stab-wound  below 
the  jaw,  showing  atrophy  of  corresponding  half  of  tongue  and 
marked  deviation  to  the  right  when  protruded. 

it  is  joined  by  branches  from  the  first  and  second  cervical  nerves, 
and  from  these  two  nerves  the  depressors  of  the  hyoid  bone  are 
supplied,  through  the  descendens  hypoglossi. 

The  symptoms  of  hypoglossal  paralysis  are  very  characteristic 
(Fig.  81).  The  corresponding  half  of  the  tongue  is  atrophied 
and  wrinkled.  When  the  tongue  is  protruded  the  healthy  side 
causes  the  tip  to  be  pushed  round  to  the  paralysed  side  in  a  sickle- 
shaped  curve.     If  the  nerve  is  divided  suddenly,  by  accident  or 


CRANIAL   NERVES  171 

operation,  the  patient  feels  for  a  few  days  as  if  tlie  paralysed  half 
of  the  tongue  were  a  foreign  body,  interfering  with  articulation 
and  mastication.  But  this  sensation  soon  passes  off  as  the  patient 
becomes  accustomed  to  his  hypoglossal  palsy. 

If  the  lesion  of  the  hypoglossal  be  extra-cranial,  after  it  has 
received  the  small  communicating  branch  from  the  cervical 
sympathetic,  we  may  sometimes  observe  vaso-motor  changes  in  the 
atrophied  side  of  the  tongue.  In  two  of  my  cases  where  the  twelfth 
was  divided  intentionally  for  the  treatment  of  facial  palsy  by 


Fig.  82. — Paralysis  of  spinal  accessory  and  hypoglossal  on  right  side,  showing- 
downward  and  outward  displacement  of  right  shoulder,  also  atrophy 
of  right  half  of  tongue  with  deviation  to  the  right  on  protrusion. 

means  of  facio-hypoglossal  anastomosis,  the  tongue  was  pale  on 
the  paralysed  side.  From  unilateral  paralysis  of  the  hyoid 
depressors,  the  larynx  may  be  pulled  over  towards  the  sound 
side  during  swallowing. 

The  hypoglossal  nucleus  within  the  medulla,  as  we  have 
already  mentioned,  is  closely  connected  with  the  lowest  cells  of  the 
facial  nucleus,  viz.,  those  which  supply  the  orbicularis  oris. 
Hence  in  lesions  in  the  neighbourhood  of  the  hypoglossal  nucleus, 
the  muscles  of  the  lips  are  paralysed  together  with  those  of  the 


172  NERVOUS    DISEASES 

tongue.  This  weakness  of  lips  and  tongue  in  nuclear  lesions  is 
generally  bilateral,  owing  to  the  close  proximity  of  the  hypoglossal 
nuclei  to  the  middle  line. 

Intra-cranial  lesions  of  the  hypoglossal  nerve,  e.g.  from  a  patch 
of  syphilitic  meningitis,  very  frequently  involve  other  cranial  nerves 
in  the  neighbourhood.  One  of  the  commonest  multiple  palsies 
is  that  which  produces  Hughlings- Jackson's  syndrome,  viz., 
hemiatrophy  of  the  tongue,  paralysis  of  the  trapezius  and  sterno- 
mastoid,  and  paralysis  of  the  vocal  cord  and  soft  palate,  all  on 
the  same  side  (Fig.  82).  This  is  the  result  of  a  lesion  implicating 
the  twelfth,  the  eleventh,  and  the  lowest  roots  of  the  tenth  nerve. 


CHAPTER   XI 

PAIN  AND   OTHER  ABNORMAL   SUBJECTIVE   SENSATIONS 

There  is,  perhaps,  no  symptom  for  which  we  are  more  frequently 
consulted  than  that  of  pain.  For  its  satisfactory  treatment  the 
underlying  cause  must  first  be  determined — sometimes  no  easy 
matter. 

With  the  exception  of  cases  where  pain  arises  in  a  healthy 
individual  from  some  unduly  strong  stimulus,  pain  is  always  patho- 
logical. The  vast  majority  of  pains  are  due  to  irritation  of  some 
peripheral  sensory  nerve  or  of  a  posterior  root.  Less  commonly 
pain  may  be  due  to  abnormal  sensitiveness  of  the  cortical  centres, 
and  is  functional  in  origin.  Stimulation  of  the  surface  of  the  brain 
gives  rise  to  no  pain,  but  the  meninges  are  exquisitely  sensitive, 
the  cerebral  membranes  being  innervated  by  the  trigeminal  nerve. 
Intra-cranial  diseases  therefore  probably  cause  pain  chiefly  through 
the  intermediation  of  the  sensitive  meninges.  It  is  possible,  how- 
ever, that  the  pain  in  some  cases  of  syringomyelia  may  not  be 
of  meningeal  origin,  but  due  to  actual  distension  of  the  syringo- 
myelic cavity  by  the  fluid  within,  though  against  this  view  is  the 
fact  that  pain  is  a  late  phenomenon  in  this  disease. 

Spontaneous  sensations  of  discomfort  vary  in  degree  and  in 
kind.  Milder  varieties,  not  amounting  to  actual  pain,  are  classed 
as  dyssestliesiae.  They  include  such  symptoms .  as  spontaneous 
tingling,  "  pins  and  needles,"  dulness,  itching,  flushing,  &c.,  whilst 
among  the  more  severe  varieties  are  the  intense  and  agonising 
pains  of  tic  douloureux,  angina  pectoris,  renal  or  biliary  colic,  or 
the  lightning-pains  of  tabes. 

In  the  diagnosis  of  the  cause  of  any  particular  dyssesthesia  or 
pain,  there  is  one  invariable  rule  which  we  should  always  follow, 
namely,  to  make  a  careful  local  examination  of  the  part  of 
the  body  to  which  the  abnormal  sensation  is  referred.     Only  in 


174  NERVOUS   DISEASES 

this  way  can  we  escape  gross  errors,  such.,  for  example,  as  that  of 
mistaking  the  pain  of  herpes  zoster  for  that  of  plem^isy.  In 
every  local  pain  we  should  first  search  for  a  local  cause,  whether 
in  the  skin,  muscles,  bones,  joints,  glands,  or  other  subjacent 
structures.  Pain  due  to  local  disease  is  usually  more  or  less 
continuous,  and  accompanied  by  objective  phenomena  such  as 
redness  of  the  skin,  sweUing  or  tenderness  of  the  diseased  tissues, 
rigidity  of  joints,  and  so  on.  The  painful  cramps  of  tetanus, 
rabies,  and  strychnia-poisoning  are  easily  recognised  and  need 
not  be  further  described. 

Some  pains  are  generalised  all  over  the  body,  for  example,  the 
pains  of  acute  illnesses  such  as  influenza,  smallpox,  and  other 
fevers  of  rapid  onset.  In  such  cases  the  elevation  of  tempera- 
ture, the  presence,  perhaps,  of  a  rash,  and  usually  the  occurrence 
of  other  similar  cases  in  epidemic  form,  all  help  us  in  the 
diagnosis. 

Intractable  paroxysmal  pains  of  hemiplegic  distribution,  in  the 
face,  trunk  and  limbs,  so-called  hemiplegia  dolorosa,  are  highly 
suggestive  of  a  lesion  localised  in  the  optic  thalamus/  In  such 
thalamic  lesions  there  is  also  hemi-ansesthesia  of  the  affected  limbs 
and  face,  together  with  spontaneous  choreiform  or  athetoid  move- 
ments and  also  hemi-ataxy  on  voluntary  movement.  These  cases 
of  hemiplegia  dolorosa  must  be  carefully  distinguished  from  the 
joint  pains  which  are  not  uncommon  in  ordinary  chronic  hemi- 
plegia, which  are  due  to  secondary  arthritic  changes  and  are  usr- 
ally  alleviated  by  massage,  hydro -therapeutics  and  anti-rheumatic 
remedies. 

Most  cases  of  pain  or  discomfort,  however,  are  localised  to 
some  more  definite  area,  and  therefore  for  diagnostic  purposes 
the  most  convenient  plan  of  studying  pains  and  other  subjective 
sensations  is  by  considering  the  different  parts  of  the  body  in  turn. 

Headache. — Cephalalgia. — ^A  diagnosis  of  "  headache  "  alone 
is  never  sufficient.  Headache  is  not  a  disease,  but  merely  a 
symptom. 

When  a  patient  complains   of   headache,  local  causes  should 

'  Dejerine  and  Roussy,  Revue  neurologique,  1906,  No.  12. 


PAIN  175 

first  of  all  be  excluded.  Amongst  tte  commonest  local  extra-cranial 
causes  we  should  bear  in  mind  rheumatic  affection  of  the  occipito- 
frontalis  muscle,  with  its  diffuse  tenderness  on  brushing  the 
hair,  and  with  aggravation  of  pain  on  movement  of  the  scalp. 
This  is  often  relieved  promptly  by  hot  applications.  Erysipelas  is 
accompanied  by  local  redness,  heat  and  oedema,  and  by  fever. 
Periostitis  of  the  pericranium  causes  tenderness  on  pressure  and  is 
often  syphilitic  in  origin,  in  which  case  the  pain  is  commonly  worse 
at  nights. 

Headaches  from  local  causes  in  the  cranial  hones  are  most 
commonly  due  to  inflammation  of  the  mucous  membrane  Hning  the 
various  air-cells,  e.g.  the  mastoid,  frontal,  or  ethmoidal  cells,  or  even 
to  an  ordinary  coryza.  Here  the  previous  history  of  the  case, 
together  with  the  local  examination,  will  serve  to  indicate  the 
cause.  Less  frequently  caries  of  the  bones  or  local  exostoses 
may  be  present.  Carious  teeth  often  cause  headache,  referred 
especially  to  the  temporal  region. 

Gross  intra-cranial  disease  may  produce  intense  headache,  either 
from  local  affection  of  the  meninges  as  in  the  various  forms  of 
meningitis  (syphihtic,  tuberculous,  or  pyogenic),  or  from  general 
increase  of  intra-cranial  pressure,  as  in  diffuse  meningitis,  intra- 
cranial abscess,  gumma,  or  tumours.  Headaches  of  intra-cranial 
origin  are  often  associated  with  the  other  classic  signs  of  increased 
intra-cranial  pressure,  especially  with  vomiting  and  optic  neuritis. 
In  every  case  of  obscure  headache  we  should  make  a  careful 
ophthalmoscopic  examination.  The  position  of  the  headache  does 
not  necessarily  correspond  with  that  of  the  tumour.  Tumours  of 
the  posterior  fossa  produce  the  most  severe  headache. 

Then  there  are  the  headaches  which  result  from  abnormahties 
of  the  intra-cranial  circulation,  especially  from  arterial  hypersemia, 
as  in  renal  disease  or  in  suppressed  menstruation,  or  temporarily 
from  drugs  such  as  nitrite  of  amyl,  erythrol  tetranitrate,  or  alcohol. 
Hypera3mia  produces  a  throbbing  pain,  sometimes  associated  with 
giddiness,  tinnitus,  affection  of  vision,  and  a  tendency  to  attacks 
of  epistaxis.  The  venous  hypersemia  of  severe  cardiac  disease  or 
of  emphysema  may  also  produce  headache,  which  is  aggravated 


176  NEKVOUS  DISEASES 

by  coughing.  The  headache  of  anaemia  is  probably  mainly  toxic 
in  origin,  rather  than  due  to  actual  deficiency  in  the  supply  of  blood 
to  the  head. 

Certain  cases  of  hemiplegia  are  preceded,  for  days  or  even 
weeks,  by  headache.  This  is  especially  common  in  cerebral  throm- 
bosis (encephalomalacia),  where  a  premonitory  headache  is  of 
considerable  diagnostic  value.  The  onset  of  a  cerebral  hcemorrhage 
is  often  coincident  with  a  headache.  Therefore  if  an  elderly  man 
complains  of  headaches  and  bleeding  from  the  nose,  we  should 
be  cautious  in  checking  epistaxis  which  may  act  as  a  safety- 
valve,  and  may  save  him  from  an  attack  of  cerebral  hsemorrhage. 

There  is  another  group  of  headaches  which  are  produced  by 
peripheral  irritation  in  various  parts  of  the  body.  Thus,  for 
example,  visceral  irritation  may  cause  headache,  as  in  "ovarian  or 
uterine  diseases,  or  in  the  headaches  from  which  so  many  women 
suffer  at  the  menstrual  periods,  and  frequently  also  throughout  the 
menopause.  In  some  people  the  swallowing  of  an  ice  causes  sudden 
frontal  headache,  when  the  ice  reaches  the  oesophagus  or  stomach. 
This  is  a  typical  "  reflex  "  gastric  headache.  Every  autumn  we  come 
across  cases  of  "  gun  headache  "  amongst  sportsmen,  not  simply  the 
result  of  the  auditory  stimulus  of  the  noise  of  the  gun,  but  due 
partly  to  the  shock  of  repeated  recoils  of  the  weapon.  Ocular 
headaches  are  fairly  frequent,  sometimes  the  result  of  disease  such 
as  glaucoma  or  iritis,  but  much  more  commonly  arising  from  errors 
of  refraction,  especially  hypermetropia  and  astigmatism.  Even 
apart  from  this,  headache  may  result  from  prolonged  eye-strain, 
e.g.  after  sight-seeing  in  picture-galleries,  being  commoner  in 
people  who  have  some  error  of  refraction. 

A  large  group  of  headaches  are  toxic  in  origin,  the  toxins 
altering  the  intra-cranial  circulation,  usually  in  the  direction  of 
raising  the  blood-pressure.  The  onset  of  certain  infective  fevers 
is  associated  with  headache,  for  example  in  smallpox  and  influenza 
(commonly  associated  with  pain  in  the  back),  in  enteric  fever 
associated  with  dyspeptic  symptoms,  in  scarlatina,  pneumonia,  &c. 
In  such  cases  the  temperature,  the  characteristic  rash,  and  the 
other   signs   and   symptoms    will   guide   us.     Poisoning   by  toxic 


PAIN  177 

substances  is  also  the  main  cause  of  the  headache  of  dyspepsia, 
whether  it  be  the  well-known  "  Katzen-jammer  " — the  bursting 
morning-headache  and  nausea  following  a  joyous  alcoholic  evening 
(this  headache,  by  the  way,  can  often  be  relieved  by  a  20-grain 
dose  of  calcium  lactate),  or  the  headache  of  chronic  dyspepsia 
especially  when  associated  with  a  constipated  intestine.  Headache 
also  results  from  poisoning  with  carbonic  oxide,  carbonic  acid 
and  other  respiratory  sewage  in  ill-ventilated  rooms  or  at  crowded 
meetings.  Other  poisons,  again,  are  autogenetic  in  origin,  as  are 
the  headaches  of  gout,  uraemia  and  diabetes. 

Sunstroke  causes  acute  diffuse  headache.  Severe  cases  are 
often  accompanied  by  other  symptoms  such  as  delirium,  hyper- 
pyrexia and  coma.  Neurasthenia  and  exhaustion,  whether  from 
overwork,  from  excessive  study  or  from  other  excesses,  are  often 
associated  with  headache,  frontal,  occipital,  or  circular  {douleur  en 
casque).  The  post-epileptic  headache  following  a  fit  is  sometimes 
severe  and  may  be  associated  with  vomiting. 

Bilateral  headaches  are  most  commonly  toxic.  The  headache 
of  dyspepsia  is  usually  referred  to  the  frontal  region,  that  of 
constipation  to  the  occiput,  whilst  vertical  headaches  are  most 
commonly  due  to  anaemia  or  to  debihty.  Some  cases  of  con- 
cussion of  the  brain  are  followed  by  obstinate  headaches,  recurring 
for  many  months.  These,  I  believe,  are  sometimes  partly  toxic 
in  origin,  a  smaller  amount  of  toxin  being  efficient  in  producing 
headache  after  concuss'on  than  in  the  case  of  a  healthy  individual, 
whilst  in  other  instances  the  headaches  occur  on  slight  mental 
exertion,  especially  where  the  patient  has  been  allowed  to  return 
to  work  prematurely.  Hence  the  importance  of  complete  physical 
and  mental  rest  after  a  severe  head  injury,  even  in  the  absence 
of  signs  of  an  organic  lesion. 

Most  of  the  headaches  to  which  we  have  referred  are  bilateral 
or  mesial  in  situation.  Let  us  now  consider  a  different  group— 
the  unilateral  or  circumscribed  pains. 

Sometimes  these  are  due  to  local  disease  of  the  scalp,  peri- 
cranium or  skull,  in  which  case  local  examination  will  generally 
reveal  the  cause.     Or  they  may  result  from  intra-cranial  disease, 

M 


178  NERVOUS    DISEASES 

for  example,  meningitis,  abscess,  gumma  or  tumour.  If  the  under- 
lying disease  be  near  the  surface  of  the  skull,  the  site  of  the  pain 
sometimes  corresponds  with  that  of  the  disease.  But  this  is  by 
no  means  always  the  case.  I  remember  a  striking  case  of  right- 
sided  cerebellar  tumour  where  the  pain  was  confined  to  the  left 
supraorbital  region.  The  growth  was  diagnosed  and  successfully 
removed. 

Some  headaches  are  associated  with  great  pallor  of  the  face 
— apparently  due  to  vaso-motor  spasm  of  the  cerebral  vessels,  often 
relieved  by  inhalation  of  amyl  nitrite.  Others  are  associated 
with  arterial  hyperssmia,  throbbing  arteries,  and  a  flushed  face. 
These  are  sometimes  promptly  reUeved  by  compression  of  the 
carotid  artery  on  the  corresponding  side.  Such  angio-neurotic 
headaches  are  rarely  bilateral. 

A  very  acute  circumscribed  variety  of  headache  is  known 
as  the  clavus  hystericus,  an  agonising  pain  usually  referred  to  the 
vertex,  as  if  a  nail  were  pressing  into  the  brain.  It  occurs  in 
certain  cases  of  hysteria  and  neurasthenia.  It  is  unassociated  with 
any  other  evidences  of  intra-cranial  disease,  and  its  very  intensity 
leads  us  to  be  suspicious  as  to  its  true  nature. 

The  pain  of  sick-headache  or  migraine  (hemicrania),  with  its 
paroxysmal  attacks  occurring  at  intervals  of  days  or  weeks,  the 
patient  during  the  intervals  being  free  from  headache,  is  usually 
easy  of  recognition.  Migraine  is  a  family  disease  which  generally 
appears  in  childhood  and  recurs  throughout  the  strenuous  period 
of  life,  tending  to  disappear  in  old  age.  The  pain  of  migraine  is 
often  alleviated  by  pressure  on  the  common  carotid  artery  of  the 
corresponding  side,  but  reappears  when  the  pressure  is  removed. 
This  headache  generally  culminates  in  vomiting,  and  is  sometimes 
preceded  by  a  visual  aura  in  the  form  of  a  scintillating  scotoma, 
consisting  of  a  blind  area  in  one  half  of  the  visual  field,  usually,  but 
not  always,  on  the  side  opposite  to  that  of  the  unilateral  headache, 
the  blind  area  being  bounded  at  its  periphery  by  a  luminous  zig-zag 
coloured  spectrum.  This  scotoma  not  infrequently  develops  into  a 
temporary  total  hemianopia.  The  headache  of  migraine  is  generally 
unilateral,  and  is  referred  to  the  side  contra-lateral  to  that  of  the 


PAIN  179 

visual  phenomena.  Thus  if  the  visual  sensations  are  in  the  left  side 
of  the  visual  fields,  the  headache  is  generally  right-sided,  and  vice 
versd.  Less  commonly  a  migrainous  attack  may  be  preceded  by  a 
non-visual  aura  of  some  sort,  e.g.,  by  a  subjective  sensation  of 
tinghng  in  one  hand  spreading  slowly  up  the  arm  to  the  face  and 
tongue,  and  followed  by  headache  on  the  opposite  side  of  the  head. 
If  the  tingling  be  right-sided  there  may  be  slight  transitory  aphasia. 
This  variety  of  migraine  is  distinguished  from  a  minor  epilepti- 
form attack  by  the  greater  intensity  and  unilateral  limitation  of 
the  migrainous  headache,  by  the  slow,  dehberate  march  of  the 
migrainous  aura,  lasting  perhaps  for  many  minutes,  by  the  absence 
of  unconsciousness,  by  the  absence  of  clonic  movements,  and  by  the 
fact,  pointed  out  by  Gowers,^  that  the  premonitory  tingling  of 
migraine  may  spread  bilaterally  to  the  tongue  and  lips,  whereas 
in  an  epileptiform  attack,  if  the  aura  spreads  to  the  tongue  or  face, 
it  remains  unilateral.  Migraine  and  epilepsy  may  alternate  in 
the  same  patient.  Migraine  ophtalmoplegique  is  a  rarer  variety, 
in  which,  in  addition  to  hemicranial  pain,  there  is  transient  paralysis 
of  the  third  nerve  on  the  same  side  as  the  headache,  with  ptosis, 
external  strabismus,  mydriasis,  &c. 

We  now  pass  to  pains  in  the  region  of  the  trigeminal  nerve. 
Of  these  tic  douloureux  is  the  most  agonising  pain  from  which 
a  patient  can  suffer.  The  pain  rarely  attacks  all  three  divisions 
of  the  nerve,  but  is  usually  confined  to  one  division  (especially 
the  supraorbital),  or  it  may  attack  two  adjacent  divisions.  The 
disease  is  hardly  ever  bilateral  except  in  cases  of  diabetes.  The 
patient  has  paroxysms  of  intolerable  agonising  pain  in  the  area 
of  the  affected  division.  During  the  attack,  the  face  is  often 
thrown  into  strong  involuntary  tonic  spasm  on  the  affected  side, 
there  is  excessive  lachrymation,  and  sometimes  secretion  of  nasal 
mucus  and  saliva,  all  on  the  affected  side.  Not  only  do  paroxysms 
occur  spontaneously,  but  the  slightest  stimuli  often  suffice  to 
induce  an  attack,  and  therefore  the  patient  avoids  chewing  food 
on  the  affected  side.  I  have  known  cases  in  which  it  was  impossible 
for  the  patient  to  wash  his  face  for  weeks  at  a  time,  lest  an  attack 

1  British  Medical  Journal,  Dec.  .3,  1906, 


180  NERVOUS    DISEASES 

should  be  thereby  precipitated.     Inveterate  trigeminal  neuralgia 
sometimes  drives  the  patient  to  suicide. 

Apart  from  these,  there  are  numerous  varieties  of  more  localised 
paroxysmal  neuralgic  pains  referred  to  individual  branches  of  the 
trigeminal  nerve,  and  associated  with  "tender  points  of  Valleix" 
over  their  foramina  of  exit.     In  such  local  neuralgias,  and  in  tic 
douloureux  itself,  we  should  always  search  carefully  for  some  local 
exciting  cause  in  the  mouth,  nose,  ear,  or  eye.    A  carious  or  inflamed 
tooth  may   cause  neuralgia    in  the  whole  of   the   corresponding 
division  of  the  fifth  nerve,  and  the  dental  surgeon  by  extracting  it 
will  relieve  the  condition.    But  we  must  beware  of  extracting  sound 
teeth  simply  because  the  patient  refers  neuralgic  pain  to  them. 
Sometimes  an  abnormally-placed  tooth,  though  healthy  in  itself, 
may  cause  neuralgia.   Thus  a  lady  of  fifty-eight  had  a  constant  burn- 
ing pain  along  the  right  side  of  her  tongue  for  eight  years,  together 
with   a  feeling  of  numbness   in   the  area  of  the  second  division 
of  the  fifth  nerve.     This  had  been  vainly  treated  by  numerous 
drugs,  whilst   all  the   time   the   real   exciting    cause    lay    in    an 
imperfectly- erupted    lower    wisdom-tooth    on    the    corresponding 
side,  the  date  of  the  pain  coinciding  with  the  first  appearance  of 
the    tooth.      Disease    of    the    antrum    or    other    accessory    air- 
sinus,    nasal    polypi,     and    other    local     lesions    may    all    cause 
localised    neuralgias.      If,    in    addition,  the    patient   be   anaemic 
or  gouty,  the  tendency  to  neuralgia  is  increased.     But   anaemia 
or  gout  alone   will  not    cause    a    local    neuralgia.      Some    local 
determining   cause   must   also   be    present,   though    it    is    some- 
times difficult  to  discover.     S5rphilitic  basal  meningitis  or  gumma, 
implicating    the    fifth    nerve    in    the    floor    of    the    skull,    may 
cause    trigeminal    neuralgia.      Such    cases    usually    show    other 
evidences  of  intra-cranial  disease,  and  we  should  look  for  signs  of 
involvement  of  the  sensory  or  motor  root  (see  page  145).     If  such 
lesions  last  any  considerable  time,  they  tend  to  produce  some 
anaesthesia  of  the  affected  nerve-area.     Localised  anaesthesia  will 
suggest  an  organic  neuritis  rather  than  a  mere  neuralgia. 

Let  us  now  consider  the  various  pains  which  may  be  met  with 
in    the  trunk.      Firstly,  there    are   the    various    root -pains,    due 


PAIN  ]81 

to  irritation  of  the  corresponding  posterior  root  or  roots  in  the 
affected  area.     Sometimes  such  root  irritation  is  due  to  disease 
of  the  spinal  meninges  (tubercle,  syphilis,  or  tumour),  to  osteo- 
arthritis, caries  or  tumours  of  the  spinal  column,  or  to  intra- thoracic 
aneurisms  and  new  growths.    Bone  pains  in  the  spine  are  associated 
with  local  tenderness  and  rigidity.     If  we  see  a  patient  supporting 
his  head  with  both  hands  owing  to  pain  in  the  neck,  this  is  almost 
pathognomonic  of  disease   of   the  cervical  vertebrse.      Root-pain 
commencing  unilaterally  and  later  becoming  bilateral  is  practically 
pathognomonic  of  a  tumour  of  the  spinal  meninges.     These  pains 
when  due  to  organic  lesions  of  the  roots,  are  not  infrequently 
associated  with  a  degree  of  hypersesthesia  or  anaesthesia  of  the 
painful   area — ancesthesia  dolorosa.     If  the   spinal   cord   be   com- 
pressed   or    infiltrated    by  the   same    lesion  as   that   which  im- 
plicates the    posteri^  roots,   we    have    evidence    of    sensory    or 
motor  paralysis   of   the   parts   below  the   lesion,  with  the  usual 
changes   in  the  reflexes,   &c.     The  girdle-pains  of  tabes  are  due 
to  affection  of  the  corresponding  posterior  roots.     Tabetic  girdle- 
pains  vary  in  degree  from  the  sensation  of  a  narrow  constrict- 
ing cord  to  one  of  a  broad  cuirass  enveloping  a  large  part  of  the 
trunk.     Such  a  cuirass  often  feels  incomplete  either  in  front  or 
behind   (Fig.   89,   p.  205).      Root-pains  may  also  occur  in  some 
cases  of  disseminated  sclerosis  {sclerosis  multiplex  dolorosa),  and 
unless  this  fact  be  borne  in  mind  a^  false  diagnosis  of  spinal  tumour 
may  be  made.^     Another  root-pain  is  that  associated  with  herpes 
zoster,  which  is  a  disease  of  the  posterior  root-ganglion.     Herpetic 
pain  is  practically  always  unilateral,  and  may  either  precede  or 
succeed  the  eruption  of  the  herpetic  vesicles.     It  may  last  for 
months  after  the  vesicles  have  disappeared.     The  pain  of  herpes 
is  often  so  sharp  that  it  may  be  mistaken  for  that  of  pleurisy,  from 
which  it  is  distinguished  by  auscultation.     Herpes  zoster  is  often 
accompanied   by   a   lymphocytosis    of    the  cerebro -spinal    fluid. 
Pleurodynia  is  a  pain  in  one  or  more  intercostal  spaces,  due  to 
a  "  rheumatic  "  myalgia  of  some  of  the  intercostal  muscles.     It 
somewhat  resembles  the  pain  of  pleurisy,  but  is  easily  distinguished 

^  Frankl-Hochwart,  Neurologisches  Centralblatt,  1906,  s.  973. 


182  NEEVOUS    DISEASES 

by  the  normal  temperature  and  by  the  absence  of  friction-sounds 
on  auscultation.  There  is  also  a  very  common  trunk-pain  which 
we  meet  with  in  people  who  are  neurasthenic  or  debihtated.  It 
is  a  deep  boring  pain,  usually  below  the  inferior  angle  of  one  or 
other  scapula.  It  is  more  difiuse  and  less  superficial  than  the 
pain  of  herpes,  and  it  has  none  of  the  physical  signs  of  pleurisy 
or  pleurodynia.  The  pain  of  traumatic  neurasthenia,  especially 
after  a  railway  or  other  accident  ("  railway  spine "),  may 
simulate  that  of  organic  spinal  lesions,  especially  when  a 
hysterical  paraplegia  coexists.  But  the  diagnosis  can  usually 
be  made  by  noting  the  excessive  hypergesthesia  of  the  spine,  the 
absence  of  signs  of  organic  disease  and  the  presence  of  various 
hysterical  "  stigmata  "  (see  later,  p.  365).  Mammary  neuralgia 
or  mastodynia  also  occurs  in  hysterical  and  neurasthenic  patients, 
and  must  be  distinguished  from  disease  of  the  gland  by  means  of 
physical  examination. 

We  have  also  to  bear  in  mind  the  various  reflected  fains 
which  may  occur  in  visceral  diseases.  Thus,  for  example,  in 
pericarditis  there  may  be  precordial  or  epigastric  pain.  Physical 
examination  will  clear  up  the  diagnosis  in  cases  of  aneurism 
and  of  mediastinal  growths.  One  of  the  most  severe  of  all 
trunk  pains  is  the  well-known  angina  fectoris.  This  is  a 
paroxysmal  suffocative  pain,  or  feeling  of  intolerable  oppres- 
sion in  the  region  of  the  heart,  often  radiating  down  one  or 
both  arms,  but  especially  down  the  left  arm.  Together  with 
this,  there  is  a  sensation  of  impending  death.  It  is  commonest 
in  male  patients  at  or  after  middle  life,  and  is  usually,  though  not 
invariably,  associated  with  evidence  of  vascular  degeneration.  It 
has  to  be  distinguished  from  toxic  or  neuralgic  angina,  so-called 
"  pseudo-angina,"  a  similar  but  much  less  serious  affection,  met 
with  most  commonly  in  young  girls,  in  women  who  have  been 
lactating  too  long,  or  in  patients  before  middle  life  who  smoke 
tobacco  or  drink  tea  to  excess. 

Irritation  of  the  sensory  nerves  at  the  gastric  end  of  the 
oesophagus,  by  abnormal  acids  or  other  irritants  in  the  stomach, 
may  cause  burning  pain,  usually  referred  to  the  seventh  left 
chondro-sternal  junction,   and   sometimes  also  to   the  left  inter- 


PAIN  183 

scapular  region.  Such  pains  are  associated  with  other  dyspeptic 
symptoms  to  which  we  need  not  here  refer  further.  As  regards  the 
situation  of  reflected  pains  in  diseases  of  various  parts  of  the  gastro- 
intestinal tract,  it  is  useful  to  bear  in  mind  Mackenzie's  rule/  that 
pain  due  to  affections  of  the  digestive  tract  is  referred  across  the 
middle  line  of  the  abdomen,  in  regularly  descending  areas  as  we  pass 
from  the  stomach  towards  the  large  intestine.  Thus  the  epigastrium 
is  the  region  for  gastric  pains  (disease  at  the  cardiac  end  causing 
pain  higher  up  than  pyloric  affections),  the  umbilical  area  is 
the  region  for  pains  of  the  small  intestine,  the  hypogastric  area 
the  site  of  pains  due  to  the  large  intestine.  A  striking  experi- 
mental corroboration  of  this  can  be  obtained  at  any  time  by 
taking  a  sharp  purgative  drug.  When  the  famiHar  colicky  pains 
appear,  they  are  felt  first  in  the  region  of  the  umbilicus,  but  soon 
they  descend  lower  and  lower,  and  when  they  arrive  close  above 
the  pubes,  the  call  for  evacuation  of  the  bowel  becomes  "  urgent 
and  imperative." 

To  discuss  fully  the  various  causes  of  acute  abdominal  pain 
would  require  many  chapters  of  description.  We  have  to  bear 
in  mind  not  only  diseases  of  the  gastro-intestinal  tract,  in  the 
form  of  catarrh,  ulcer,  muscular  spasm,  &c.,  but  also  perforations 
of  various  hollow  viscera,  the  stomach,  gall-bladder,  intestines 
(including  the  vermiform  appendix),  rupture  of  a  pyo-salpinx 
or  of  a  tubal  pregnancy,  biliary  or  renal  colic,  acute  pancreatitis, 
torsion  of  an  ovarian  pedicle,  &c.  In  every  instance,  not  only 
should  we  carefully  examine  the  whole  abdomen,  but  we  should, 
if  necessary,  examine  the  pelvis,  'per  rectum  or  per  vaginam,  and 
investigate  the  urine  and  dejecta. 

Apart  from  acute  renal  colic,  a  floating  kidney  is  a  fairly  common 
cause  of  diffuse  abdominal  pain,  especially  in  poorly-nourished 
women  with  lax  abdominal  walls.  Here  again,  local  examination 
of  the  abdomen  will  reveal  the  cause. 

Before    leaving    the    subject    of    abdominal    pains,    we    must 

not  fail  to   recall   the   familiar  crises  of  tabes   dorsalis  : — gastric 

crises  associated  with  pain  and  vomiting,  intestinal  crises  associated 

with    colic    and    diarrhoea,    diaphragmatic    crises    with  hiccough, 

1  Brain,  1901,  vol.  xxv.  p.  373. 


184  NERVOUS    DISEASES" 

bladder  crises,  &c.  All  these  may  closely  simulate  the  pain  of 
acute  abdominal  disease.  But  the  history  of  the  case,  together 
with  an  investigation  of  the  pupils,  knee-  and  ankle-jerks,  and 
the  other  phenomena  of  tabes,  will  usually  save  us  from  error. 

Lumbago,  or  pain  in  the  lumbar  muscles,  a  variety  of 
myalgia,  is  usually  easily  recognised.  The  pain  is  intensified 
by  active  muscular  contraction  and  also  by  passive  stretching, 
caused  for  instance  by  the  stooping  posture.  It  is  also  associated 
with  tenderness  on  pressure.  Lumbo-abdominal  neuralgia,  on 
the  other  hand,  is  a  diffuse  and  more  superficial  pain,  not  confined 
to  the  lumbar  region  but  spreading  forwards  to  the  front  of 
the  abdomen,  and  sometimes  to  the  groin,  genitals  or  gluteal 
region.  It  is  paroxysmal,  and  during  the  paroxysm  there  may 
be  cramp-like  spasms  of  the  abdominal  muscles  or  of  the  cremaster. 
It  is  associated  with  the  "  tender  points  "  of  a  true  neuralgia, 
these  being  situated  over  the  vertebral  spines,  the  iliac  crests,  the 
linea  alba,  inguinal  canal,  scrotum  or  labium.  Sacral  pain  is  often 
due  to  uterine  disease,  as  in  the  famihar  uterine  dysmenorrhoea 
or  the  well-known  pains  of  labour. 

Coccygodynia  or  neuralgic  pain  in  the  region  of  the  coccyx,  is 
practically  confined  to  the  female  sex.  The  pain  may  be  spon- 
taneous, or  it  may  be  induced  by  sitting  or  walking  or  by  the  con- 
traction of  any  of  the  muscles  attached  to  the  coccyx,  e.g.  during 
defgecation.  It  is  often  associated  with  local  tenderness.  Before 
making  a  diagnosis  of  mere  neuralgia,  local  disease  of  the 
coccyx  or  of  adjacent  structures  must  always  be  excluded  by 
local  examination,  both  externally  and  fer  rectum. 

Pains  in  the  Limbs. — Brachial  neuralgia,  generally  a  uni- 
lateral affection,  is  referred,  as  a  rule,  to  the  whole  area  of  distribu- 
tion of  the  plexus,  namely  to  the  lower  part  of  the  neck,  the 
shoulder  and  the  whole  upper  limb,  being  most  intense  in  the 
proximal  part  of  the  limb.  It  is  raie  to  meet  with  neuralgia 
confined  to  an  individual  nerve-area,  such  as  that  of  the  median 
or  uhiar,  except  in  cases  of  local  injury  or  disease  of  the  nerve- 
trunks.  The  pain  of  brachial  neuralgia  is  aggravated  by  move- 
ment of  the  limb,  which  feels  heavy  and  numb,  though  there  is  no 


PAIN  185 

paralysis.  The  "  tender  points  "  are  over  the  nerve-trunks,  such 
as  the  musculo-spiral,  circumflex,  median  or  ulnar  nerves. 

If  anaesthesia  or  trophic  changes  be  superadded,  we  probably 
have  to  do  with  structural  changes  in  the  nerve-trunk,  that  is, 
with  a  neuritis,  not  a  mere  neuralgia.  In  every  case  of  brachial 
neuralgia  we  must  carefully  examine  the  nerve-trunks  in  their 
entire  course,  to  exclude  the  possibility  of  organic  lesions  com- 
pressing or  infiltrating  the  nerves.  In  addition  to  pain,  brachial 
neuritis  often  produces  weakness  and  atrophy  of  the  corre- 
sponding muscles,  and  impairment  or  perversion  of  cutaneous 
sensation. 

Analogous  to  brachial  neuralgia  and  neuritis  in  the  upper  limb, 
we  have  in  the  lower  limb  sciatica,  a  term  which  includes  sciatic 
neuralgia  and  sciatic  neuritis.  In  every  case  of  so-called  sciatica 
we  have  to  decide  which  of  these  two  is  present.  In  sciatic 
neuralgia  there  is  usually  a  dull  aching  pain,  more  or  less  constant, 
in  the  back  of  the  thigh,  with  occasional  paroxysms  of  darting  or 
boring  pain,  generally  from  above  downwards,  along  the  course 
of  the  sciatic  nerve.  Any  movement  of  the  limb  whereby  the 
nerve  is  made  tense,  or  any  local  pressure  as  from  sitting  on  a  hard 
chair,  brings  on  a  paroxysm.  Therefore  the  patient  habitually 
keeps  the  hip  and  knee  slightly  flexed  on  the  affected  side,  so  as 
to  relax  the  nerve.  It  is  not  uncommon  to  find  a  slight  degree 
of  scoliosis  in  the  lumbar  region,  the  concavity  being  towards  the 
sound  side.  The  "  tender  points  "  are  at  the  fifth  lumbar  spme 
(especially  on  lateral  pressure  from  the  affected  towards  the 
healthy  side  ^)  over  the  posterior  ihac  spine,  the  sciatic  notch, 
the  popliteal  space,  the  peroneal  nerve  below  the  head  of 
the  fibula,  and  behind  the  malleoli.  Passive  stretching  of  the 
nerve  increases  the  pain,  for  example  by  flexion  of  the  hip  with 
the  knee  extended.  Blunting  of  sensation  in  the  peroneal  or  pos- 
terior tibial  area  is  uncommon  and  indicates  an  organic  neuritis  or 
perineuritis,  as  also  do  any  alterations  in  the  electrical  reactions 
of  the  muscles,  or  any  considerable  degree  of  muscular  atrophy. 
In  sciatic  neuritis  the  temperature  of  the  limb  is  generally  lower 

^  Raimist,  Neurolog.  Centralbl.,  1909,  p.  1087. 


186  NERVOUS    DISEASES 

than  on  the  healthy  side.  The  ankle-jerks  should  always  be 
tested  on  both  sides.  In  sciatic  neuritis  the  jerk  may  be 
diminished  or  lost,  whereas  in  neuralgia  it  remains  normal.  In 
both  affections  we  may  observe  exaggeration  of  the  cremasteric 
reflex  on  the  affected  side. 

Meralgia  parcesthetica  is  a  variety  of  neuralgia  occurring  in  the 
area  of  distribution  of  the  external  cutaneous  nerve  of  the  thigh. 
It  consists  in  parsesthesia  or  actual  pain  in  the  outer  aspect  of  one 
thigh.  The  pain  is  often  induced  by  standing  or  walking,  possibly 
owing  to  stretching  of  the  fascia  lata.  In  some  cases  it  results 
from  the  pressure  on  the  nerve  by  a  badly-fitting  corset.  It  is 
sometimes  associated  with  flat-foot  on  the  same  side.  Here,  as 
in  brachial  or  sciatic  pain,  the  presence  of  an  area  of  impaired 
sensation  would  indicate  a  neuritis  rather  than  a  neuralgia. 

In  rare  cases  we  may  find  neuralgia  in  the  area  of  the  anterior 
crural  or  of  the  obturator  nerve,  and  this  may  be  symptomatic  of 
an  intra-pelvic  tumour,  or  of  an  obturator  hernia. 

The  pains  of  brachial  or  sciatic  neuralgia  and  neuritis,  and  of 
meralgia  paraesthetica,  are  unilateral.  Let  us  now  consider  the 
bilateral  pains  which  may  be  met  with  in  the  limbs. 

Bilateral  pains  should  always  suggest  to  our  minds  either  a- 
toxic  cause  attacking  the  peripheral  nervous  structures  of  both 
limbs,  or  some  central  disease  of  the  spinal  meninges  affecting  the 
posterior  roots  bilaterally,  or  again  some  angio -neurotic  condition 
such  as  Raynaud's  disease,  erythromelalgia,  or  intermittent  limp. 

Pains  in  the  muscles  or  joints  are  a  common  symptom  in  people 
who  work  under  compressed  air,  as  in  divers  or  workers  in  deeply 
sunk  caissons,  whether  under  ground  or  under  water.  The 
symptoms  of  caisson  disease,  or  "  decompression  paraplegia,"  are 
most  likely  to  occur  when  the  worker  ascends  too  abruptly  to  the 
ordinary  atmosphere.  All  such  workers  ought  to  pass  through 
a  "  decompression-chamber,"  where  the  atmospheric  pressure  is 
gradually  reduced  to  normal.  If  this  be  not  done,  bubbles  of 
nitrogen  are  set  free  in  the  blood  and  may  either  form  emboli 
in  the  arterioles  of  the  central  nervous  system  with  consequent 
small  foci  of  necrosis,  or  the  nitrogen  may  effervesce  out  of  the 


PAIN  -         187 

capillaries  into  the  nervous  tissues,  especially  into  the  substance  of 
the  spinal  cord.  Capillary  hsemorrhages  may  also  occur.  Clinically 
in  such  cases  not  only  have  we  severe  pains  in  the  limbs  but 
also  aural  symptoms  due  to  labyrinthine  affection  : — deafness, 
giddiness  and  tinnitus,  sometimes  even  actual  rupture  of  the 
tympanic  membrane.  There  may  also  be  anaesthesia  and  para- 
plegia of  spinal  type,  and  such  paralysis  may  be  permanent. 
Slighter  cases  clear  up  quickly,  if  the  air-extravasation  has  been 
merely  from  the  capillaries  without  air-embolism  of  the  arterioles. 

The  lightning  fains  of  tabes  may  be  unilateral  or  bilateral. 
They  are  commoner  in  the  legs  than  in  the  arms,  since  tabes  is  a 
disease  which  generally  begins  in  the  posterior  root-fibres  of  the 
lumbo-sacral  region.  These  pains  are  variously  described  by  the 
patient  as  stabbing,  burning,  tearing,  or  bursting,  and  are  commonly 
associated  with  local  hypersesthesia  of  the  skin.  They  are  frequently 
mistaken  for  rheumatic  pains,  and  all  the  more  so  inasmuch  as 
they  often  coincide  with  changes  in  the  weather. 

Tight  "  tourniquet "  pains  around  the  lower  limbs,  in  broad 
zones  rather  than  narrow,  are  sometimes  an  early  and  persistent 
symptom  in  disease  of  the  lumbo-sacral  region  of  the  cord.  They 
are  due  to  irritation  of  the  posterior  roots,  and  may  also  occur  in 
tabes.  Koot -pains  also  occur,  though  less  commonly,  in  certain 
cases  of  multiple  sclerosis. 

The  root-pains  of  tumour  or  inflammation  of  the  spinal  men- 
inges, or  of  spinal  caries,  are  more  or  less  constant,  with  paroxys- 
mal exacerbations.  Inflammatory  affections  of  the  meninges  are 
usually  bilateral  from  the  outset,  with  corresponding  bilateral  pains. 
But  in  cases  of  meningeal  tumour  the  pains  are  generally  unilateral 
at  first,  and  become  bilateral  as  the  disease  spreads  to  the  opposite 
side.  The  level  of  the  pains  in  meningeal  disease  varies  with  the 
level  of  the  affected  posterior  roots.  Thus  in  cervical  meningitis, 
tumour  or  caries,  there  is  pain  in  the  neck,  spreading  down  one  or 
both  arms  along  the  corresponding  root-areas ;  in  thoracic  cases 
the  pain  is  around  the  trunk,  and  in  lumbar  or  sacral  cases  it  is  in 
various  parts  of  the  lower  limbs.  Meningeal  pain  is  often  asso- 
ciated with  local  hypersesthesia  corresponding  to  the  uppermost 


188  NERVOUS    DISEASES 

roots  affected,  and  with  tonic  spasms  of  the  muscles  at  that  level. 
If  the  mieningeal  lesion  affects  the  cord  within,  whether  by  com- 
pression or  by  infiltration,  there  will  be  in  addition  to  root -pains  the 
other  signs  of  organic  cord  disease — so-called  'paraplegia  dolorosa, 
with  its  anaesthesia,  motor  weakness  and  alterations  of  reflexes 
below  the  level  of  the  lesion.  Inflammatory,  tuberculous  and 
syphilitic  affections  of  the  spinal  meninges  are  always  associated 
with  cellular  changes  in  the  cerebro-spinal  fluid  (see  p.  411). 

Affections  of  the  peripheral  nerves  may  also  produce  pain. 
Thus  in  peripheral  neuritis  there  is  not  only  pain,  with  hypersesthesia 
of  the  skin  of  the  feet  and  hands,  but  there  is  intense  muscular 
tenderness  on  pressure,  together  with  a  degree  of  tactile  anaesthesia, 
and  in  severe  cases  muscular  paralysis  and  muscular  atrophy, 
accompanied  by  the  reactions  of  degeneration. 

Pains  localised  in  single  nerve-areas  should  always  lead  us  to 
examine  the  nerve-trunk  in  its  entire  extent.  Tubercula  dolorosa 
are  multiple  growths  (usually  neuro-fibromata)  in  the  connective 
tissue  of  the  nerve-trunks,  many  of  them  forming  little  subcutaneous 
nodules  easily  palpable  and  exquisitely  tender,  others  less  acces- 
sible in  the  deeper  nerve-trunks,  causing  referred  pains  in  the 
particular  nerve  areas.  If  these  growths  not  merely  irritate  but 
interrupt  the  nerve-fibres  within  the  nerve-trunks,  there  may 
in  rare  cases  be  areas  of  anaesthesia.  Clinically  we  seldom  find 
motor  paralysis  from  such  growths,  except  as  a  result  of  pressure 
on  the  spinal  cord  or  base  of  the  brain  by  a  neuroma  on  one  of  the 
spinal  or  cranial  nerve-roots. 

It  is  convenient  here  to  refer  to  erythromelalgia,  where  there  are 
cyanosis  and  pain  in  one  or  both  feet  in  the  dependent  posture, 
relieved  by  elevating  the  limb  ;  to  Raynaud's  disease,  which  may  be 
associated  not  only  with  local  pallor,  cyanosis  or  gangrene,  but  also 
with  subjective  sensations  of  tingling  or  pain  ;  and  to  intermittent 
limp,  when  the  patient  after  a  few  steps  becomes  unable  to  walk 
farther,  owing  to  intolerable  pain  in  the  muscles  of  the  leg.  To 
these  conditions  we  shall  return  later,  when  studying  the  ner- 
vous affections  of  the  vascular  system. 

Paroxysmal   spontaneous   pain  in   the   periphery  of   a   limb, 


PAIN  189 

ascending  towards  the  trunk,  sometimes  occurs  as  a  variety  of  sen- 
sory fit  in  gross  disease  of  the  cortical  sensory  areas  in  the  contra- 
lateral post-central  gyrus.  Thus  in  one  case  of  my  own,  where 
there  was  a  focal  lesion  of  the  lef  b  post -central  gyrus,  the  earliest 
symptom  was  paroxysmal  pain  in  the  right  fingers  and  hand.'^ 

Finally,  we  should  refer  to  the  group  of  pains  met  with  in 
hysteria  and  neurasthenia.  These  are  more  often  areas  of  hyper- 
aesthesia  than  of  spontaneous  pain.  They  are  specially  common 
in  the  neighbourhood  of  joints,  whose  slightest  movement  causes 
intense  pain.  In  other  cases  the  muscles  are  apparently  hyper- 
sensitive, so  that  any  attempt  at  movement  of  the  limb,  active 
or  passive,  causes  an  illusion  of  pain — so-called  akinesia  algera, 
of  psychical  origin.  But  the  history  of  the  case,  in  which  there 
has  often  been  a  preceding  local  injury,  the  absence  of  signs  of 
structural  disease,  local  or  central,  and  the  presence  of  other 
hysterical  or  neurasthenic  phenomena,  will  aid  us  in  our  diagnosis. 
It  may  be  necessary  to  give  a  general  anaesthetic  in  order  to 
eliminate  gross  local  organic  disease. 

^  Review  of  Neurol,  and  Psychiatry,  1908,  p.  379. 


CHAPTER  XII 

ABNORMALITIES   OF   SENSATION: 
HYPERJESTHESIA,   PARESTHESIA,   ANESTHESIA 

We  have  already  considered  the  anatomical  course  of  the  chief 
sensory  paths  from  the  periphery  to  the  perceiving  centres  in  the 
brain  (Chapter  I.).  Let  us  now  proceed  to  consider  the  methods 
of  clinical  investigation  of  the  various  forms  of  sensation. 

All  parts  of  the  surface  of  the  body  are  not  equally  sensitive. 
Thus  the  tip  of  the  tongue,  the  lips,  the  finger-tips,  in  the  order 
mentioned,  are  most  sensitive  to  cutaneous  impression,  whilst 
other  parts  such  as  the  dorsal  aspect  of  the  trunk,  the  upper  arm, 
and  the  calf  of  the  leg,  are  least  sensitive.  These  differences  de- 
pend on  various  factors,  such  as  thickness  of  epithelium,  relative 
abundance  of  sensory  end-organs,  &c.,  into  which  we  need  not 
enter  more  minutely  here. 

All  sorts  of  ingenious  apparatus  have  been  devised  for  the 
accurate  measurement  of  minute  differences  in  sensibility  to  touch, 
pressure,  pain,  temperature,  and  so  on.  But  for  clinical  diagnosis, 
we  should  avoid  complicated  apparatus  and  content  ourselves 
with  the  simplest  possible  methods  which,  while  accurate  enough 
for  practical  purposes,  do  not  impose  too  great  a  strain  on  the 
patient's  attention  nor  demand  too  high  a  degree  of  intelHgence 
on  his  part. 

The  most  important  varieties  of  sensory  stimuli  which  we 
employ  in  testing  a  patient's  sensory  functions  are  hght  touches, 
pin-pricks,  cold  and  hot  objects,  all  of  which  refer  to  cutaneous 
sensations.  We  have  also  to  consider  other  sensations,  such  as 
joint-sensation  (or  sense  of  position  on  passive  movement),  active 
muscle- sensation  (kineesthetic  sense,  or  sense  of  active  muscula  • 
contraction)  and,  lastly,  the  vibration  sensation  produced  when  a 
sounding  tuning-fork  is  placed  over  the  subcutaneous  surface  of 

190 


ABNOEMALITIES    OF    SENSATION  191 

a  bone  or  upon  a  finger-nail.  There  are  other  varieties  of  sensory 
stimuU,  such  as  electro-cutaneous  sensibihty  (which  is  generally, 
but  not  always,  parallel  in  intensity  with  the  pain-sense),  and 
there  is  the  sensation  of  pressure  and  appreciation  of  differences 
of  pressure,  &c.  But  these,  though  physiologically  interesting,  are 
of  minor  clinical  value. 

There  is  perhaps  no  better  criterion  of  neurological  dexterity 
than  the  accuracy  with  which  an  observer  can  map  out  areas  of 
diminution  or  loss  of  sensation  on  the  one  hand,  or  of  perverted 
or  exalted  sensation  on  the  other.  Both  experience  and  patience 
are  required,  in  order  to  obtain  trustworthy  results. 

Inasmuch  as  we  are  largely  dependent  on  the  intelligence  and 
goodwill  of  our  patient  for  accurate  answers,  we  must  as  far  as 
possible  try  to  eliminate  all  distracting  outside  factors.  Therefore 
we  direct  the  patient  to  close  his  eyes  when  we  are  testing 
sensation,  so  that  his  attention  may  not  be  diverted  by 
watching  what  is  being  done.  We  must  also  be  careful  not 
to  weary  a  patient  by  too  prolonged  examination,  lest  as 
he  gets  tired  or  impatient  his  answers  become  inaccurate.  The 
simpler  our  methods  of  examination,  the  better  are  our  results 
likely  to  be.  We  have  also  to  contend  with  wide  variations  in 
the  intelhgence  of  different  patients,  in  their  education,  and  in 
their  attentiveness ;  this  latter  may  be  modified  by  pain,  by 
anxiety,  or  by  psychical  deficiencies.  Sometimes  we  have  to 
deal  with  deliberate  attempts  on  the  part  of  the  patient  to  mislead 
us.  Fortunately,  patients  who  simulate  disease  generally  make 
blunders  so  gross  as  to  prevent  an  erroneous  diagnosis  on  the 
part  of  a  careful  observer.  Of  course  the  physician  must  be  care- 
ful to  avoid  suggesting  the  presence  of  sensory  changes  to  the 
patient  under  examination. 

Clinical  Investigation  of  Sensation. — At  the  start,  the 
patient's  eyes  should  be  closed,  or  some  object  should  be  inter- 
posed between  his  eyes  and  that  part  of  the  body  which  is  being 
tested.  We  then  proceed  to  test  the  various  cutaneous  sensations — 
touch,  pain  and  temperature,  separately  and  in  turn. 

Touch  is  tested  by  means  of  some  soft  light  object,  such  as  a 


192  NERVOUS    DISEASES 

tuft  of  cotton-wool,  a  feather,  or  by  gentle  pulling  or  stroking  of 
the  hairs.  Loss  of  sensation  in  the  hairs  is  called  "  tricho- 
ansesthesia."  Pressure  is  tested  by  means  of  a  pencil  or  other 
blunt  object ;  if  such  pressure  be  steadily  increased  a  "  deep  " 
sensation  of  pain  is  ultimately  produced.  Cutaneous  fain  is 
tested  by  pricking,  or  better  by  scratching,  with  a  sharp  needle  ; 
cold  by  blowing  on  the  skin,  or  by  a  cold  object  such  as  a  metal 
spoon  or  a  test-tube  containing  ice-cold  water  ;  heat  by  breathing 
on  the  skin  or  by  a  warm  object  such  as  a  test-tube  containing 
hot  water. 

Each  Variety  of  sensation  should  be  examined  separately,  before 
passing  on  to  the  next  kind  of  stimulus,  and  the  results  should  be 
recorded  on  an  outhne-chat  of  the  body.  In  mapping  out  areas 
of  abnormal  sensation,  it  is  useful  to  have  a  skin -pencil  with  which 
to  mark  the  patient's  skin,  before  copying  the  result  on  our  chart. 

An  important  practical  point  in  mapping  out  areas  of  ansesthesia, 
is  to  begin  within  the  anaesthetic  area,  and  to  work  towards  the 
normal  skin,  not  in  the  reverse  direction.  It  is  easier  for  a  patient 
to  recognise  the  moment  when  he  first  feels  a  sensation  than  for 
him  to  observe  when  he  first  loses  it.  On  the  other  hand,  in 
mapping  out  areas  of  hypersesthesia  or  of  parsesthesia,  we  should 
work  from  normal  skin  towards  the  hypersesthetic  area,  asking 
the  patient  to  call  out  as  soon  as  his  sensation  changes. 

In  setting  about  the  examination  of  the  sensory  functions,  we 
usually  begin  with  that  of  touch.  The  patient's  eyes  being  closed, 
we  touch  him  lightly  on  both  sides  of  the  face  simultaneously 
and  observe  not  only  whether  he  feels  the  touches,  but  whether 
they  are  equally  distinct  on  the  two  sides.  We  then  touch  sym- 
metrical spots  on  the  neck,  shoulders,  hands,  trunk,  and  lower  limbs. 
We  next  proceed  to  do  the  same  with  light  needle-scratches,  then 
with  cold  and  with  warm  objects.  If  the  patient  has  an  area  of 
diminished  or  altered  sensibility,  we  generally  discover  it  by  this 
method.  When  we  find  an  area  of  abnormality,  we  proceed  to  map 
it  out  carefully,  making  separate  observations  for  touch,  pain,  and 
temperature,  and  noting  whether  the  areas  coincide  or  overlap. 

Besides  noting  whether  a  patient  feels  a  stimulus,  for  instance  a 


ABNORMALITIES    OF    SENSATION  193 

tactile  one,  we  should  also  notice  whether  he  localises  it  accurately. 
This  is  accomplished  by  asking  him  to  place  his  finger  on  the  spot 
where  he  was  touched,  for  instance,  the  dorsum  of  the  hand.  A 
normal  individual  can  do  this  accurately  to  within  a  fraction  of  an 
inch.  But  in  certain  varieties  of  ansesthesia,  the  patient,  whilst 
able  to  tell  that  he  has  been  touched,  makes  an  error  of  several 
inches  in  locahsation.  This  is  called  "  atopognosis."  Horsley  ^ 
maintains  that  errors  in  the  localisation  of  cutaneous  impressions 
are,  in  cases  of  cortical  lesions,  always  in  a  proximal  direction,  i.e. 
the  patient  refers  the  stimulus  to  a  point  higher  up  the  limb. 
Sometimes  the  patient,  when  touched  on  one  side  of  the  body, 
feels  the  sensation  at  the  corresponding  spot  on  the  opposite 
side.  This  is  termed  "  allocheiria,"  and  occurs  chiefly  in  certain 
cases  of  hysteria. 

When  testing  pain,  we  sometimes  find  that  though  the  patient 
correctly  perceives  and  localises  the  stimulus,  there  is  an  abnormally 
long  interval  of  time,  perhaps  amounting  to  several  seconds,  be- 
tween the  stimulus  and  the  patient's  perception  of  pain.  This  is 
called  "  delayed  sensation,"  and  is  met  with  chiefly  in  cases  of  tabes. 

When  charting  areas  of  very  slight  cutaneous  anaesthesia,  it  is 
often  difficult,  despite  the  utmost  care  as  regards  our  stimuli,  to 
obtain  an  exact  outline  of  the  area  of  altered  sensibility.  Changes 
in  the  quality  of  sensations  may  exist  which  are  undetectable 
even  by  cotton-wool  touches.  Nevertheless  the  patient,  if  he 
tests  his  own  skin,  may  be  conscious  of  an  abnormality  too  delicate 
to  be  discovered  by  another  person  on  objective  examination. 
But  if  we  have  a  specially  intelligent  patient  and  get  him  to  explore 
his  anaesthetic  area  by  stroking  with  his  own  finger,  indicating 
where  he  perceives  a  line  of  transition  between  normal  and  abnormal, 
it  is  often  possible  for  him,  by  such  "  auto-exploration,"  to  map 
out  the  area  of  altered  sensibility  with  great  accuracy.^ 

So  much  for  cutaneous  sensations.  But  there  are  other  forms 
of  sensation  which  are  of  clinical  importance.  Joint-sense  is  tested 
by  moving  a  joint  passively  into  various  positions  backwards  and 

1  Brain,  1906,  p.  137. 
2  Trotter  and  Davies,  Rev.  of  Neurol,  and  Psych.,  1907,  p.  761. 

N 


194  NERVOUS    DISEASES 

forwards,  then  holding  it  fixed  in  a  certain  position,  such  as  that 
of  semi-fiexion,  and  asking  the  patient  to  imitate  exactly  that 
position  with  the  limb  of  the  opposite  side.  It  not  infrequently 
happens  that  when  a  patient  is  in  doubt  as  to  the  position  of  his 
joint,  he  begins  to  make  slight  voluntary  movements  of  the  joint 
before  answering.  These  must  not  be  permitted,  since  he  thereby 
gains  information  as  to  the  position  of  the  limb,  not  from  his  joint- 
sense  but  through  an  entirely  different  sense,  viz.,  the  kinsesthetic 
sense  or  sense  of  active  muscular  contraction. 

To  test  this  Mncesthetic  sense,  we  notice  whether  the  patient,  when 
raising  his  limbs,  can  detect  differences  in  the  weights  of  objects 
of  similar  size,  for  example  a  shilhng  and  a  sovereign,  either 
placed  in  his  hand,  or  hung  in  a  sling  over  his  hand  or  foot.  For 
this  purpose  we  sometimes  employ  a  series  of  leather  or  wooden 
balls  of  equal  size,  loaded  with  different  weights.  Normally, 
according  to  Weber's  law,  a  healthy  individual  should  detect  an 
increase  of  one-third  in  the  weights  of  two  successive  objects. 
Tabes  is  the  disease  in  which  this  sense  of  active  muscular  con- 
traction is  most  markedly  diminished,  and  where  the  joint-sense 
is  notably  impaired  also.  The  loss  of  these  two  senses  is  probably 
the  main  factor  in  the  production  of  tabetic  ataxy. 

We  purposely  avoid  using  the  term  "  muscular  sense,"  for 
several  reasons.  Firstly,  it  is  ambiguous,  since  it  has  been  used  to 
include  two  entirely  different  senses  : — joint-sense  and  kinaesthetic 
sense.  Moreover,  it  might  also  be  confounded  with  a  third  sense, 
the  sensibility  of  muscles  to  pressure  with  the  fingers.  Normally 
such  pressure,  if  moderate  in  degree,  is  painless  ;  but  in  certain 
diseases,  as  in  peripheral  neuritis,  in  the  various  forms  of  myositis, 
and  in  the  abdominal  muscles  superficial  to  an  area  of  peritonitis, 
the  muscles  become  exquisitely  tender  to  the  lightest  pressure. 
On  the  other  hand,  it  is  common  to  find  in  tabes  that  severe  com- 
pression of  the  muscles  and  tendons,  for  example  of  the  leg 
muscles,  and  especially  of  the  tendo  Achillis,  is  painless  (Abadie's 
sign).  This  muscle  and  tendon  analgesia  is  often  present  in 
early  stages  of  the'  disease. 

It    is    sometimes  of    value   to  observe  the   patient's  power  of 


ABNORMALITIES    OF    SENSATION 


195 


recognising,  without  seeing  them,  the  forms  of  soHd  objects  placed 
in  his  hand — so-called  stereognostic  'perception.  Normally  a  patient 
should  be  able  to  recognise  familiar  objects  such  as  a  key,  a  coin, 
or  a  chain.  But  in  some  cases  the  patient,  though  able  to  feel 
the  presence  of  some  object,  cannot  describe  its  form  and  qualities, 
without  seeing  it.  Such  "  astereognosis  "  may  be  due  to  impair- 
ment of  sensation  either  from  peripheral  disease,  from  thalamic 
lesions,  or  from  disease  in  the  cortical  centres. 

Lastly,  there  is  the  vibration-sense  (pallsesthesia,  or  "  osseous 
sense  ")  described  originally  by  Egger.  This 
is  tested  by  means  of  a  low-pitched  tuning- 
fork,  which  is  set  into  vibration  and  placed 
upon  the  subcutaneous  surface  of  a  bone. 
In  normal  individuals  a  characteristic  vibratile 
thrill  is  felt.  But  in  certain  diseases  involv- 
ing the  posterior  roots,  such  as  tabes,  or  in 
transverse  lesions  of  the  spinal  cord,  the 
vibration-sense  may  be  lost  in  the  bones 
corresponding  to  the  affected  roots  (Fig.  83). 
Loss  of  this  sense  may  be  the  earliest  form  of 
anaesthesia  in  root-lesions  as  in  tabes,  where 
it  sometimes  precedes  cutaneous  anaesthesia. 
In  Brown-Sequard  paralysis  vibration-sense 
is  lost  on  the  same  side  as  the  muscular 
paralysis  ■*  (see  Figs.  10  and  13).  But  the  vibration-sense  is  not 
an  exclusive  property  of  bones,  though  bones  are  most  strikingly 
sensitive  ;  it  can  be  perceived  in  other  tissues,  notably  in  the 
nails,  which  are  closely  connected  with  the  periosteum,  and  even 
in  the  connective-tissues,  though  in  them  less  intensely. 

Excessive  sensitiveness  to  normal  stimuli  is  termed  hyper ces- 
thesia.  Such  hyperaesthesia  is  usually  accompanied  by  a  degree 
of  discomfort  or  even  pain,  even  though  a  stimulus  be  used  which 
is  ordinarily  painless.  The  term  parcesthesia,  or  perversion  of 
sensation,  signifies  that  an  ordinary  stimulus  evokes  an  unusual 
sensation,  as  for  example  a  feeling  of  tingling  when  the  skin  is 

1    Vide  Bing,  Neurolog.  Gentralhlatt,  1910,  p.  173. 


Fig.  83. — Tabeswith  loss 
of  vibration-sense  in 
bones  of  lower  limbs, 
pelvis,  lumbar,  and 
lower  dorsal  vertebrae. 
The  bones  with  loss 
of  vibration-sense  are 
shaded  black. 


196  NERVOUS   DISEASES 

touched,  or  a  feeling  of  acute  pain  when  moderate  cold  is  applied. 
Under  the  head  of  parsesthesise  we  may  also  include  such  pheno- 
mena as  multiple  sensations  (polysesthesia),  allocheiria,  &c. 

Strictly  speaking,  diminution  of  sensation  should  be  designated 
hypo-CBsthesia,  and  the  term  anaesthesia  should  be  reserved  for  total 
loss  of  sensation.  It  is  usual,  however,  to  speak  of  "  slight," 
"  moderate,"  and  "  total "  anaesthesia.  When  only  one  form  of 
cutaneous  anaesthesia  is  referred  to,  we  sometimes  find  it  con- 
venient to  talk  of  tactile  ancesthesia,  of  analgesia  or  loss  of  pain- 
sense,  and  of  thermo-ancBsthesia  or  loss  of  temperature -sense. 
Dissociated  ancesthesia  is  where  some  forms  of  sensation,  such  as 
tactile  sense,  are  normal,  whilst  in  the  same  area  others,  such 
as  pain  and  temperature -sense,  are  lost.  This  occurs  especially 
in  syringomyeha  and  in  the  Brown-Sequard  syndrome. 

We  speak  of  hemi-ancBsthesia  where  one-half  of  the  body,  right 
or  left,  is  affected,  and  of  para-ancesthesia  where  both  legs  or  both 
arms  are  affected  owing  to  a  lesion  of  the  spinal  cord  or  to  a 
symmetrical  affection  of  the  posterior  roots.  We  also  speak  of 
radial,  ulnar,  peroneal  anaesthesia,  &c.,  where  the  sensory  loss 
corresponds  to  the  distribution  of  a  single  peripheral  nerve. 

Hyperaesthesia. — Universal  hyperaesthesia  is  rare.  It  is 
chiefly  met  with  in  hysteria,  but  also  occurs  in  other  affections,  as 
in  strychnia-poisoning,  where  the  slightest  touch  may  suffice  to 
evoke  a  violent  spasm.  Hemi-hyperaesthesia  is  chiefly  found  in 
neurasthenic  and  hysterical  patients  and  may  be  associated  with 
other  hysterical  "  stigmata."  Thus  I  remember  the  case  of  a 
soldier  with  traumatic  hysteria  who  had  hemi-hyperaesthesia, 
accompanied  by  abnormal  widening  of  the  visual  field  and  by 
increased  acuity  of  smell,  taste,  and  hearing,  all  on  the  hyper- 
aesthetic  side  of  the  body. 

In  the  thalamic  syndrome,  hemi-hyperaesthesia  to  temperature 
and  pain  sometimes  coexists  with  hemi-anaesthesia  to  tactile  stimuli 
and  with  impairment  of  joint  sense,  loss  of  osseous  sense  and 
astereognosis  in  the  affected  limbs. 

Hyperaesthesia  in  more  or  less  symmetrical  root-areas  of  the 
trunk  or  limbs,  due  to  irritation  of  the  posterior   roots,   is  not 


ABNOKMALITIES    OF    SENSATION  197 

uncommon  in  diseases  causing  pressure  on  the  spinal  cord  or  its 
meninges,  as  in  caries  or  tumours  of  ttie  spine.  Here  the  hyper- 
sesthesia  corresponds  to  the  area  suppUed  by  the  uppermost  root 
involved,  and  is  usually  associated  with  anaesthesia  and  motor 
weakness  in  the  parts  below. 

Odd  irregular  areas  of  hypersesthesia  are  amongst  the 
commonest  stigmata  of  hysteria,  and  do  not  correspond  either  to 
root-areas  or  to  the  distribution  of  peripheral  nerves.  Tender 
areas  are  particularly  common  over  hysterical  joints  and  over 
certain  vertebral  spines  in  hysteria,  and  we  frequently  notice  that 
the  lightest  touches  cause  severe  pain,  whereas,  when  the  patient's 
attention  is  diverted,  deep  pressure  on  the  same  spot  may  be 
painless.  Pressure  on  such  tender  spots  may  sometimes  excite  a 
hysterical  attack — "  hysterogenic  "  areas — and  in  other  cases  may 
restrain  or  stop  an  attack — "  hysterofrenic "  areas.  To  this 
subject  we  shall  return  when  discussing  the  diagnosis  of  hysteria. 

Next  in  frequency  after  hysterical  hypersesthesia  are  the  areas 
of  cutaneous  hypersesthesia  in  tabes.  Tactile  hypersesthesia  is 
specially  common  in  cases  with  gastric  or  other  visceral  crises, 
in  the  root-areas  corresponding  to  the  viscus  affected.  It  is 
also  common  in  the  areas  where  Hghtning-pains  are  felt,  and 
like  these  pains  it  may  be  one  of  the  earliest  evidences  of  the 
disease.  Thus  a  patient  with  incipient  tabes,  for  years  before 
he  reached  the  stage  of  ataxia,  was  so  hypersesthetic  around  the 
trunk  that  it  was  agony  for  him  to  pull  his  shirt  on,  or  to  sponge 
his  body  when  bathing.  Tabetic  hypersesthesia  may  occur  not 
only  on  the  trunk  but  also  on  the  limbs,  and  even  on  the  face. 
Hypersesthesia  is  specially  frequent  round  the  orbits  in  cases 
of  tabetic  ocular  palsies. 

Hypersesthesia  in  the  areas  of  peripheral  nerves  occurs  in  the 
true  neuralgias,  as  in  trigeminal  neuralgia,  where  the  neuralgic 
area  is  often  exquisitely  tender,  especially  over  the  foramina  of 
exit  of  the  various  branches.  The  patient  may  be  unable  to 
wash  his  face  for  weeks  at  a  time,  since  the  lightest  touches 
induce  a  paroxysm  of  neuralgia.  Localised  hypersesthesia  some- 
times precedes  the  eruption  of  herpes  zoster,  and  may  persist  for 
weeks  or  months  after  the  eruption  has  passed  away.      Lastly, 


198 


NERVOUS    DISEASES 


we  may  mention  the  hyperaesthesia  of  the  hands  and  feet  in 
multiple  neuritis,  where  there  is  often  present  a  degree  of  anaesthesia. 
The  coexistence  of  hyperalgesia  to  light  pressure  with  anaesthesia 
to  light  touches  is  very  characteristic  of  alcoholic  neuritis. 


FiCt.  84. — Universal  aiiEesthesia  in  a  hysterical  patient.  Sterilised 
safety-pins  have  been  pushed  through  the  skin  on  both  sides 
without  producing  bleeding.     Hysterical  contracture  of  left  hand 

is  also  present. 

Parse  sthesia,  or  perverted  sensation,  has  much  the  same  diag- 
nostic significance  as  hyperaesthesia.  It  may  also  be  mentioned 
that  when  a  peripheral  cutaneous  nerve  is  in  process  of  recovery 
after  an  injury,  there  is  often  a  stage  of  paraesthesia  through 
which  the  skin  passes  before  normal  sensation  is  restored. 


ABNORMALITIES    OF    SENSATION  199 

Anaesthesia. — Universal  anaesthesia  of  the  skin  and  accessible 
mucous  membranes  to  all  forms  of  stimuli  is  exceedingly  rare, 
occurring  only  in  hysteria.  Fig.  84  shows  such  a  case  in  a  girl,  in 
whom  it  was  possible  to  push  pins  through  the  skin  on  both 
sides  of  the  body  without  causing  pain. 

Hemi-anaesthesia  always  indicates  a  central  affection.  In  every 
case  of  hemi-anaesthesia  we  must  determine  whether  the  disease  is 
functional  or  organic,  and  if  organic,  at  what  level  in  the  sensory 
tract  the  lesion  is  situated,  whether  in  the  cortex,  internal  capsule, 
or  lower  down. 

Hysterical  hemi-ancesthesia  is  commoner  than  organic.  It  varies 
in  degree,  from  total  anaesthesia  down  to  the  shghtest  degree  of 
comparative  blunting  of  sensation,  only  discoverable  on  com- 
parison of  the  two  sides.  Not  uncommonly  it  tends  towards  the 
"  segmental "  type,  and  it  is  frequently  accompanied  by  other 
hysterical  stigmata,  especially  by  blunting  of  the  special  senses  on 
the  hemi-anaesthetic  side,  particularly  by  concentric  contraction 
of  the  visual  field,  and  by  other  features  which  we  shall  study 
later.  We  should  remember  that  hysteria  sometimes  coexists 
with  organic  disease,  thereby  comphcating  the  diagnosis. 

Organic  hemi-ancesthesia  may  also  vary  in  its  degree,  from  slight 
to  severe  anaesthesia ;  but  it  is  never  absolute  in  degree  as  in  some 
cases  of  hysteria.  It  is  generally  more  marked  on  the  limbs 
than  on  the  trunk  or  face,  and  more  intense  at  the  periphery  of 
a  limb  than  at  its  proximal  end.  It  is  never  marked  off  by  a 
sharp  line  running  across  the  limb,  as  in  the  "  segmental " 
anaesthesia  of  hysteria,  but  fades  gradually  in  intensity  as  we 
pass  from  the  hand  to  the  shoulder.  A  degree  of  atopognosis  is 
always  present  in  organic  hemi-anaesthesia.  The  special  senses 
are  unaffected  (their  paths  probably  do  not  traverse  the  internal 
capsule),  with  one  exception,  namely  that  of  vision,  in  cases  where 
the  lesion  implicates  the  optic  radiations.  But  here  again  we  get 
a  homonymous  hemianopia,  unlike  the  hysterical  contraction  of 
the  visual  field  to  which  we  shall  refer  later. 

If  we  find  that  a  hemi-anaesthesia  is  organic  in  origin,  we  have 
then  to  determine  whether  the  lesion  is  cortical  in  situation   or 


200  NERVOUS    DISEASES 

whether  it  is  lower,  in  the  internal  capsule,  optic  thalamus,  or  else- 
where. In  cortical  hemi-ansesthesia  the  other  signs  of  cortical 
disease  will  aid  the  diagnosis.  The  presence  of  monoplegia  rather 
than  hemiplegia,  or  the  occurrence  perhaps  of  Jacksonian  fits,  will 
point  to  a  cortical  localisation,  remembering  that  the  cortical 
motor  areas  are  also  partly  sensory.  Cortical  anaesthesia  is  less 
profound  than  capsular,  and  is  most  distinct  at  the  periphery  of 
the  affected  limb.  Indeed,  in  cortical  anaesthesia  it  is  the  rule  for 
the  trunk  to  be  little  or  not  at  all  affected.  Marked  astereognosis 
and  atopognosis  with  but  slight  tactile  and  motor  loss  will  also 
point  to  a  cortical  lesion,  probably  in  the  upper  parietal  region. 

Capsular  hemi-ansesthesia  (which,  by  the  way,  is  generally  the 
result  of  a  lesion  not  actually  in  the  capsule  but  in  the  postero- 
external part  of  the  optic  thalamus)  is  never  monoplegic  in  type 
but  always  affects  the  entire  half  of  the  body,  including  the  trunk. 
Hemi-ansesthesia  from  a  thalamic  lesion,  as  we  have  seen,  is 
associated  with  paroxysmal  pains  of  intolerable  severity  in  the 
affected  limbs  and  side  of  the  face,  and  sometimes  with  hemi- 
hypersesthesia  to  pain  and  temperature.  The  thalamic  syndrome 
also  includes  hemi-ataxy  of  the  limbs  and  spontaneous  choreiform 
or  athetoid  movements.  The  deep  reflexes  are  unaffected,  and 
the  plantar  reflex  remains  of  the  normal  flexor  type,  since  the 
pyramidal  motor  path  is  intact.  Such  cases  often  have  a  history 
of  transient  motor  hemiplegia  at  the  onset,  but  this  motor  weakness 
rapidly  disappears  and  is  succeeded  by  paroxysmal  pains  in  the 
hemi-ansesthetic  limbs  and  face.  The  intensity  of  capsular  or 
thalamic  anaesthesia  is  deeper  than  in  cortical  cases,  but  not  so 
markedly  intensified  at  the  periphery  of  the  limbs.  It  is  associated 
with  hemianopia  if  the  lesion  extend  backwards,  or  with  motor 
hemiplegia,  most  marked  in  the  leg  (but  not  a  monoplegia),  if 
the  lesion  extend  forward  into  the  pyramidal  motor  path. 

We  may  also  have  hemi-anaesthesia  from  organic  lesions  of  the 
sensory  path  below  the  level  of  the  optic  thalamus ;  in  fact,  at 
any  level  above  the  sensory  (fillet)  decussation  in  the  medulla. 
Such  lesions,  although  uncommon,  can  be  correctly  localised 
by   the   coexistence    of    other   signs.       Thus   a   unilateral    lesion 


ABNORMALITIES    OF    SENSATION  201 

in  the  dorsal  aspect  of  the  potis,  implicating  the  trigeminal  nerve  or 
nucleus,  together  with  the  remainder  of  the  sensory  fibres  belonging 
to  the  other  side  of  the  body,  will  cause  a  crossed  hemi-anoBsthesia, 
i.e.  ansesthesia  of  the  face  on  the  side  of  the  lesion,  and  of  the  arm, 
trunk,  and  leg  on  the  opposite  side  (Fig.  12,  p.  18).  A  lesion  of 
the  sensory  path  in  the  medulla  below  the  level  of  the  trigeminal 
nerve,  must  be  more  widespread  laterally  to  produce  a  com- 
plete hemi-ansesthesia,  since  the  path  for  temperature  and  pain 
is  here  at  some  distance  from  the  tactile  path  (Fig.  11,  p.  17). 

Anaesthesia  also  occurs  in  certain  lesions  of  the  spinal  cord.  We 
should  note,  however,  that  there  are  many  cord  diseases  in  which 
anaesthesia  is  absent,  such  as  progressive  muscular  atrophy, 
amyotrophic  lateral  sclerosis  and  acute  anterior  poliomyelitis. 
Disseminated  sclerosis  is  also  a  disease  in  which  sensory  changes  are 
frequently  absent.  But  if  the  spinal  cord  be  destroyed  or  divided 
at  a  certain  transverse  level,  whether  by  trauma  or  by  disease 
such  as  acute  softening,  whereby  sensory  as  well  as  motor  paths  are 
interrupted,  all  the  sensory  impressions  ascending  in  the  posterior 
and  lateral  columns  (Figs.  8  and  10,  pp.  10  and  14)  will  be  lost 
below  the  level  of  the  lesion.  We  then  have  a  para-ancesthesia,  the 
upper  limit  of  which  corresponds  with  that  of  the  highest  sensory 
root  affected.  And  since  in  many  of  these  cases  there  are  irritative 
or  inflammatory  processes  affecting  the  roots  immediately  above  the 
area  of  destruction,  it  not  unfrequently  happens  that  there  is  a 
narrow  zone  of  parsesthesia  or  of  hypersesthesia  immediately 
above  the  anaesthetic  area.  In  cases  where  the  cord  is  gradually 
compressed  by  progressive  disease  in  the  meninges  or  vertebrae, 
there  is  usually  a  progressive  paraplegia  with  the  usual 
alteration  of  reflexes.  Here  anaesthesia  appears  late  in  the  dis- 
ease, being  preceded  by  spontaneous  subjective  sensations  or  dys- 
CBsthesice,  after  which  hyperaesthesia  appears,  and  last  of  all 
anaesthesia.  The  anaesthesia  of  a  total  transverse  lesion  implicates 
all  forms  of  sensation,  both  superficial  and  deep. 

When  a  cord  lesion  is  incomplete  in  its  transverse  extent,  certain 
forms  of  sensation  may  escape.  Thus  unilateral  lesions  of  the  cord 
produce  Brown- Sequard  paralysis .    Most  commonly  this  is  the  result 


202  NERVOUS    DISEASES 

of  a  stab  or  bullet-wound,  but  it  may  also  be  caused  by  softenings 
or  growths.  Or  a  lesion  which  was  originally  more  extensive,  e.g. 
a  haemorrhage,  may  clear  up  so  as  to  become  a  unilateral  one.  In 
the  typical  Brown-Sequard  syndrome,  as  will  be  seen  from  Figs.  10 
and  13,  there  are  on  the  side  of  the  lesion  the  well-known  motor 
and  vaso-motor  paralyses,  together  with  loss  of  sensation  in  the 
joints  and  muscles  and  loss  of  vibration-sense,  whilst  on  the  opposite 
side  there  are  thermo-ansesthesia,  analgesia  and  some  tactile  anaes- 
thesia. In  thermo-ansesthesia  from  cord  lesions,  the  areas  of 
anaesthesia  to  cold  and  to  heat  are  sometimes  co-extensive.  But 
this  is  not  always  so  ;  sensibility  to  heat  may  be  abolished  without 
loss  of  sensibility  to  cold,  or  vice  versa,  or  the  areas  of  loss  to  heat 
and  to  cold  may  differ  widely  in  extent.  If  the  lesion  be  above 
the  lumbar  enlargement,  as  is  generally  the  case,  the  motor 
paralysis  is  of  the  upper  neurone  type,  with  spasticity,  increased 
deep  reflexes  and  an  extensor  type  of  plantar  reflex.  If,  as  some- 
times happens  in  stab-wounds,  the  lesion  destroys  the  most  lateral 

region  of  the  cord  but  does  not  quite 
reach  the  middle  line,  thereby  sparing 
the  postero -internal  column,  the  deep 
structures  on  the  side  of  the  lesion 
preserve  their  sensibility.  In  any  case, 
on  the  side  of  the  lesion,  a  narrow  zone 
of  anaesthesia  exists,  corresponding  to 
the  posterior  root-fibres  cut  across  at 
the  level  of  the  lesion.  And  above  the 
anaesthesia  there  is  a  zone  of  hyper- 
FiG.  85.-SyriDgomyelia,  indi-  gggthesia  from  irritative  root-changes. 

catmg  area  of  thermo-anses-  _  '^^ 

thesia  and  analgesia  in  the         Dissociated  ancBsthesia,  often  without 

patient  shown  in  Fig.  86.  .         .  ,      •   ,-         i 

motor  paraplegia,  is  characteristic  oi 
disease  in  the  region  of  the  posterior  cornua  of  the  cord  or  in 
the  substantia  gelatinosa  of  the  medulla,  as  in  syringomyelia 
and  syringobulbia,  where  there  are  analgesia  and  thermo-antes- 
thesia,  with  loss  of  vibration-sense,  corresponding  to  the  area 
of  spinal  cord  affected,  whilst  tactile  sensation  remains  unim- 
paired (see  Fig.  85).    The  patient  often  burns  his  fingers  accidentally 


ABNORMALITIES    OF    SENSATION 


203 


without  pain,  and  he  may  develop  painless  whitlows  in  his 
analgesic  fingers — so-called  Morvan's  disease.  He  may  also  have 
spontaneous  joint  disintegrations,  with  fractures  and  osteophytic 
or  destructive  changes  in  the  articular  ends  of  the  bones.  In 
most  cases  of  syringomyelia  there  also  is  some  atrophy  of  the 
anterior  cornua ;  we  should  therefore  be  on  the  look-out  for  a 
coexisting  muscular  atrophy  of  spinal  type,  involving  especially 
the    small    muscles    of    the    hands.      If     the    pyramidal    tracts 


Fig.  86. — Syringomyelia  with  arthropathy  of  right  shoulder-joint 
and  scoliosis. 

become  involved  in  syringomyelia,  a  spastic  paraplegia  is  super- 
added, and  sooner  or  later  a  degree  of  scoliosis  or  even  kypho- 
scoliosis develops  (Fig.  86). 

But  unilateral  cord  lesions  and  syringomyelii  are  not  the  only 
diseases  which  produce  dissociated  anaesthesia.  A  small  lesion 
such  as  an  area  of  softening  or  of  new  growth,  in  the  ponto-cerebellar 
angle  of  the  pons  at  the  level  of  the  auditory  nerve,  will  cause 
deafness  of  the  same  side  with  analgesia  and  thermo-ansesthesia 
of  the  opposite  side,  tactile  sensation  being  unaffected.  If  the 
cerebellar  peduncle  be  involved,  there  will  be  cerebellar  phenomena 
also,  such  as  we  have  already  studied. 

Tabetic  ancesthesia  is  the  commonest  of  all  organic  ansesthesise. 


204 


NERVOUS    DISEASES 


In  this  disease  the  sensory  loss  tends  to  follow  fairly  closely  the 
distribution  of  the  posterior  roots  afiected  by  the  tabetic  process. 
Thus  it  is  commoner  in  the  lower  limbs  than  in  the  upper.  Joint- 
sense  and  vibration-sense  usually  become  impaired  earlier  than 
cutaneous  sensations,  whilst  analgesia  precedes  tactile  anaesthesia. 
In  the  upper  limbs  the  fingers  on  the  ulnar  side  of  the  hand  are 
usually  affected  earlier  than  the  other  digits,  and  there  is  often 

a  strip  of  analgesia  running  longitudin- 
ally along  the  inner  side  of  the  whole 
upper  hmb,  corresponding  to  the  eighth 
cervical  and  first  thoracic  roots  (Fig.  87). 
In  many  tabetics  the  ulnar  nerve  behind 
the  elbow  loses  its  normal  sensitiveness 
on  pressure — ^Biernacki's  sign.  And  on 
the  trunk  it  is  common  to  find  a  broad 
zone    of    analgesia,    and  sometimes   of 

tactile   ansesthesia   as   well,   the   upper 
Fig.   87.-Early  tabes     show-    ^^^^^^   ^f   ^j^-^j^   -g   ^^   ^^^^   jg^gi  of  ^^le 
ing  '   cuirass      or  subjective 
girdle-feeling  (clotted  area)  second  ribs  in  front.     This  zone  is  often 

with     zone      of     cutaneous  .     ,        . 

hypersestbesia     below     the  incomplete  laterally  or  posteriorly,  just 

cuirass,  passing  up  between  ,i  r,-     j.-  u       •  55      „^   „4-;^^ 

itslimitsposterioiiy(crosses).   as  the   subjective      cuirass      sensation 
Analgesic  areas   (horizontal  ^g^^  ^g_     Analgesia  of  the  glans  penis 

shading)  in  upper  limbs  (Cg  ''  ^    _  ox 

and  Thj  roots)  and  in  lower  is  another  early  sign  of  tabes,  also  loss 

limbs  (Li,  L.3,  and  Si  roots).  „,  i,i  Pii^j-i 

of  the  normal  tenderness  01  the  testicle 
on  pressure.  Tendinous  analgesia,  on  pinching  the  tendo  AchilUs 
(Abadie's  sign),  is  also  present  in  the  majority  of  tabetic  patients. 
But  tabetic  anaesthesia  is  not  always  sharply  limited  to  root 
areas,  and  we  should  seek  for  confirmatory  evidence  of  the  disease 
in  the  pupils,  deep  reflexes,'  cerebro -spinal  fluid,  &c. 

Anaesthesia  in  peripheral  nerve  palsies  of  sensory  or  mixed 
nerve-trunks,  is  of  course  confined  to  the  distribution  of  the 
affected  nerve  or  nerves.  If  a  cutaneous  nerve  be  paralysed  we 
have  loss  of  "  epicritic "  and  "  protopathic "  cutaneous  sensa- 
tions, whilst  the  deep  sensibility  in  muscles,  bones  and  tendons 
is  still  preserved  (see  p.  14).  If  a  mixed  nerve-trunk  be 
paralysed,  muscular  paralysis  with  atrophy  is  added  to  anaesthesia, 


ABNORMALITIES    OF    SENSATION 


205 


both  cutaneous  and  deep,  and  the  diagnosis,  as  a  rule,  presents 
no  difficulties.  It  must  be  borne  in  mind  that  as  a  mixed  nerve 
recovers  from  its  paralysis,  sensation  usually  returns  before  motor 
power  and  protopathic  sensation  before  epicritic.  The  anaesthesia 
following  an  attack  of  herpes  zoster  sometimes  lasts  for  a  consider- 
able time  after  the  eruption  has  disappeared.  In  the  anaesthesia 
of  multiple  neuritis,  whether  resulting  from  alcohol,  diphtheria, 
diabetes,  septic  poisoning,  or  other  causes,  the  disease  is  generally 


Fig.  88. — From  a  case  of  multiple 
neuritis,  showing  "glove"  and 
"  sock"  areas  of  antesthesia. 


Fig.  89. — From  another  case  of 
peripheral  neuritis,  showing 
"  glove  "  and  "  stocking  "  areas 
of  cutaneous  parsesthesia. 


bilateral  and  symmetrical,  affecting  hands  or  feet  or  both.  Sub- 
jective tingling  sensations  usually  precede  the  anaesthesia,  which 
is  of  the  "  glove  "  and  "  sock  "  variety,  not  marked  off  sharply 
as  in  the  "  segmental "  anaesthesia  of  hysteria,  but  shading  off 
gradually  at  the  upper  margin  (see  Figs.  88  and  89).  Most  cases 
have  also  some  superadded  motor  weakness  in  the  form  of  drop- 
foot  and  drop -wrist.  Lead  paralysis  differs  from  ordinary  peri- 
pheral neuritis  in  being  entirely  a  motor  palsy,  free  from  sensory 
changes,  and  whilst  affecting  the  muscles  innervated  by  the 
musculo-spiral  nerve,  it  usually  leaves  the  supinator  longus  un- 
impaired. Moreover,  the  extensor  communis  is  less  severely 
paralysed  than  the  extensor  indicis  and  extensor  minimi  digiti. 


CHAPTER   XIII 

OEGANIC  MOTOR  PARALYSIS  OF  UPPER  NEURONE  TYPE 

In  the  investigation  of  the  various  motor  palsies,  apart  from  those 
affecting  the  cranial  nerves  which  we  have  already  studied,  we 
should  proceed  in  a  definite  order. 

We  commence  by  inspection  of  the  palsied  limb  or  Hmbs,  noting 
the  posture  of  the  limb,  the  presence  or  absence  of  local  mus- 
cular atrophy  or  hypertrophy,  the  existence  of  pathological  swell- 
ings, &c.  We  then  proceed  to  palpation  of  the  bones  and  joints, 
following  their  outhnes  and  testing  their  range  of  passive  move- 
ment, so  as  to  discover  whether  the  deficiency  of  active  movement 
may  not  be  due  to  mechanical  causes,  such  as  fractures,  disloca- 
tions, ankyloses,  adhesions  or  inflammations  of  bones  or  joints, 
and  so  on.  Thus  in  the  case  of  a  semi-comatose  lady,  whom  I  saw 
within  a  few  hours  after  a  carriage  accident,  there  was  apparent 
inabihty  to  move  the  left  arm  or  leg.  This  might  have  suggested 
a  lesion  of  the  right  cerebrum  producing  hemiplegia,  but  a  pre- 
Hminary  investigation  of  the  bones  showed  that  the  left  femur  and 
left  clavicle  were  broken.  It  was  therefore  unnecessary  to  diagnose 
an  intra-cranial  lesion  of  the  pyramidal  tract,  especially  as  the 
plantar  reflexes  were  normal  on  both  sides.  The  result  proved 
the  correctness  of  this  view. 

We  should  also  observe  whether  the  muscles  of  the  affected 
part  are  rigid,  stiff  and  spastic,  or  whether  they  are  loose,  relaxed 
and  flaccid. 

Lastly,  we  proceed  to  investigate  the  patient's  powers  of  volun- 
tary movement  of  the  affected  Hmb.  In  doing  this,  it  is 
not  enough  to  tell  the  patient  in  general  terms,  to  "  move  the 
arm,"  and  so  on.  We  should  test  each  joint  and  each  movement 
separately,  fixing  the  proximal  part  of  the  hmb  and  instructing 
the  patient   to   perform  various   movements  :— flexion,  extension, 


PARALYSIS    OF    UPPER    NEURONE    TYPE  207 

rotation  inwards  and  outwards,  &c.,  separately  and  distinctly. 
Thus,  for  example,  when  we  direct  a  patient  to  pronate  his  fore- 
arm, we  must  fix  the  humerus  and  see  that  he  does  not  abduct 
the  shoulder  to  make  up  for  deficiency  in  pronation.  To 
determine  whether  a  particular  muscle  is  taking  part  in  a  move- 
ment or  not  sometimes  requires  very  close  observation,  not 
only  by  inspection  but  by  palpation  of  the  muscle  or  of  its 
tendon.  But,  as  Beevor  has  remarked,^  the  physician  "  must 
avoid  the  error  of  assuming  that  the  tightening  of  a  tendon  from 
the  stretching  of  a  passive  muscle  is  evidence  of  contraction  of 
the  muscle." 

Suppose  that  a  particular  movement  of  a  limb  is  deficient, 
we  estimate  the  deficiency  in  different  ways,  according  to  its  degree. 
If  the  weakness  is  shght,  we  detect  it  by  interposing  some  resist- 
ance, so  as  to  load  the  muscles.  This  is  accomphshed  either  by 
means  of  weights,  or,  in  the  case  of  the  hand,  by  making  the 
patient  squeeze  our  hand  or  compress  an  oval  spring-dynamometer, 
or,  in  the  case  of  the  leg,  by  holding  the  hmb  down  and  making 
him  elevate  it  against  resistance. 

If  the  weakness  is  more  marked,  it  can  be  detected  without 
loading  the  muscles.  The  weight  of  the  distal  part  of  the  limb 
may  already  be  too  nmch  for  the  muscles  to  lift,  as,  for  example, 
in  cases  of  drop-wrist  and  drop-foot,  due  to  weakness  of  the  ex- 
tensors of  the  wrist  and  dorsiflexors  of  the  foot.  But  even  in 
these,  a  minimal  degree  of  voluntary  contraction  may  perhaps 
still  be  present,  and  can  still  be  detected  by  placing  the  limb  pas- 
sively in  such  a  posture  that  its  own  weight  is  no  longer  a  factor, 
e.g.  by  testing  the  extensors  of  the  wrist  with  the  forearm  midway 
between  pronation  and  supination,  or  testing  the  movements  of 
the  elbow  by  passively  abducting  the  upper  arm  and  getting  the 
patient  to  flex  and  extend  his  elbow  in  a  horizontal  plane.  Or  we 
may  even  observe  the  hmb  when  it  is  supported  on  all  sides  by 
water,  as  in  a  warm  bath.  In  this  way  we  may  detect  minimal 
movements.  And  in  such  cases  we  watch  carefully,  not  only  for 
movement  of  the  joint,  but  for  contraction  of  the  tendons  of  the 

1  Croonian  Lectures,  1904,  p.  4. 


208  NERVOUS    DISEASES 

muscles  concerned.  These  latter  may  sometimes  be  felt  to  con- 
tract, when  they  are  too  feeble  to  overcome  the  inertia  of  the 
joint. 

By  inspection  and  palpation  we  also  note  whether  in  the  affected 
limb  the  muscles  are  normal  in  volume  and  firmness,  whether  some 
are  enlarged  and  stronger  than  usual — hypertrophy — or  whether 
some  are  diminished  in  size — atrophy,  so  that  there  is  flattening, 
or  even  hollowing,  in  place  of  the  normal  muscular  contour.  In 
some  cases,  an  apparent  increase  in  volume  is  accompanied  by 
weakness  of  the  enlarged  muscles — so-called  pseudo-hypertrophy. 

If  a  muscle  is  atrophied,  its  electrical  reactions,  both  to 
faradic  shocks  and  to  the  continuous  galvanic  current,  should  be 
investigated.  The  reactions  may  be  normal,  or  they  may  be 
merely  quantitatively  diminished.  Or  they  may  be  qualitatively 
altered,  as  in  the  "reactions  of  degeneration"  (see  later,  p.  401). 
Or  they  may  be  "  mixed,"  where  some  fibres  of  the  muscle  are 
normal,  whilst  others  intermingled  with  them  are  degenerated. 

Reaction  of  a  muscle  to  direct  percussion  is  sometimes  of  value. 
This  phenomenon  consists  in  a  contraction  of  the  whole  bundle 
of  muscle-fibres  in  their  entire  length.  Response  to  direct 
mechanical  excitation  often  persists  when  the  deep  reflexes  are 
lost ;  thus,  for  example,  when  the  knee-jerk  is  absent  in  tabes 
or  peripheral  neuritis,  the  quadriceps  still  responds  to  direct  tapping. 
In  most  cases  of  lower  motor  neurone  lesion,  this  mechanical 
irritability  of  the  muscle-fibres  is  increased  but  the  contraction  is 
more  flickering  than  in  a  healthy  muscle.  In  muscular  dystrophy, 
the  mechanical  irritability  is  lost  in  the  affected  muscles.  In 
certain  patients,  especially  on  percussing  the  pectorals  or  other 
flat  muscles  of  the  chest,  we  may  observe  a  wave  of  contraction 
dashing  outwards  suddenly  in  both  directions  from  the  point 
of  percussion,  longitudinally  along  the  muscular  fibres,  and  imme- 
diately followed  by  a  temporary  small  muscular  swelling  at 
the  point  of  percussion.  This  phenomenon  is  called  myoidema; 
it  is  common  in  pulmonary  tuberculosis,  but  occurs  also  in  many 
other  wasting  conditions  not  associated  with  muscular  paralysis, 
and  need  not  detain  us  further. 


PARALYSIS    OF    UPPER    NEURONE    TYPE  209 

The  term  paralysis,  when  apphed  to  voluntary  muscles, 
signifies  loss  of  the  power  of  voluntary  contraction,  due  to  inter- 
ruption, functional  or  organic,  in  any  part  of  the  motor  path,  from 
the  cerebral  coitex  down  to  and  including  the  muscle-fibre.  This 
latter  part  of  the  definition  is  necessary  so  as  to  exclude  such 
cases  as  ankylosed  joints,  where  movement  is  impossible  from 
mechanical  reasons  without  true  paralysis.  Strictly  speaking, 
paralysis  is  total  loss  of  voluntary  motor  power,  lesser  degrees  of 
impairment  being  called  paresis.  But  we  often  employ  the 
term  paralysis  to  include  partial  as  well  as  complete  loss  of 
power. 

The  distribution  of  motor  weakness  differs  according  to  the 
site  of  the  lesion  of  the  motor  path.  Thus  in  a  unilateral 
brain  lesion,  there  is  usually  paralysis  of  one  side  of  the  body, 
including  the  face,  trunk  and  limbs.  This  is  termed  hemi- 
plegia.  A  bilateral  cerebral  lesion  produces  diplegia  or  double 
hemiplegia,  the  limbs  on  both  sides  of  the  body  being  affected. 
Paralysis  of  a  single  limb  resulting  from  a  cerebral  lesion  is 
termed  cerebral  monoplegia.  Spinal  or  peripheral  monoplegia  is 
less  common. 

Paralysis  of  the  limbs  resulting  from  a  lesion  of  the  spinal  cord 
is  most  commonly  bilateral — paraplegia — and  usually  affects  the 
legs  alone ;  but  if  the  lesion  be  in  the  cervical  region,  it  affects 
both  arms  and  legs.  It  must  be  distinguished  from  a  cerebral 
diplegia,  in  which  the  face  is  sometimes  also  affected.  In  rare 
cases  both  arms  may  be  paralysed  from  a  spinal  lesion,  with  little 
or  no  affection  of  the  legs  ;  this  is  brachial  paraplegia.  A  uni- 
lateral spinal  lesion  may  also  cause  a  monoplegia,  but  this  is  un- 
common. The  term  crossed  or  alternate  hemiplegia  means  that  as 
a  result  of  a  single  lesion  there  is  paralysis  of  some  parts  on  the 
right  side  and  of  others  on  the  left.  For  example,  a  lesion  in 
the  right  side  of  the  pons  at  the  level  of  the  facial  nerve  will 
cause  paralysis  of  the  right  side  of  the  face  and  of  the  left  arm 
and  leg.  There  are,  of  course,  other  varieties  of  crossed  paralysis. 
When  paralysis  is  due  to  a  lesion  of  a  peripheral  nerve,  it 
may  either  be  asymmetrical,  when  the  motor  weakness  is  limited 

o 


210  NERVOUS    DISEASES 

to  one  or  more  nerve-trunks,  as  in  most  traumatic  nerve-palsies, 
or  more  commonly  bilateral  and  symmetrical,  as  in  the  various 
forms  of  toxic  neuritis,  affecting  either  the  upper  or  lower  or  all 
four  limbs. 

If  paralysis  be  due  to  primary  affection  of  the  muscles 
themselves,  as  in  the  myopathies,  its  distribution  is  usually  bilateral, 
and  it  affects  all  four  limbs  and  sometimes  even  the  face. 

We  must  remember  that  it  is  not  uncommon  to  meet  with 
multiple  lesions  in  a  single  case  ;  yet,  in  diagnosis,  it  should  always 
be  our  endeavour  to  try  to  account  for  all  the  symptoms  by  a 
single  lesion. 

Suppose,  then,  that  a  patient  is  suffering  from  motor  paralysis 
(mechanical  impediments  having  been  excluded),  the  first  ques- 
tion is — Is  the  paralysis  functional  or  organic?  If  it  is  organic, 
we  proceed  to  the  further  questions — Where  is  the  lesion  situated  ? 
(anatomical  diagnosis),  and  what  is  its  nature  ?  (pathological 
diagnosis). 

Is  the  Paralysis  Functional  or  Organic  ? — Sometimes  the 
distinction  between  functional  and  organic  motor  paralysis  is 
easy ;  at  other  times  it  is  a  matter  of  considerable  difficulty, 
cases  of  early  disseminated  sclerosis  being  particularly  liable 
to  be  mistaken  for  hysteria ;  moreover,  it  is  possible  to  have 
a  combination  of  functional  and  organic  disease  in  the  same 
patient. 

More  detailed  consideration  of  the  diagnostic  features  of 
hysteria  will  be  postponed  till  a  later  chapter  (see  p.  361),  and  we 
shall  only  here  refer  to  some  of  the  main  features  which  enable  us 
to  decide  that  a  case  is  organic  rather  than  functional.  Firstly,  the 
history  of  the  case  often  guides  us ;  for  instance,  functional 
paralysis  frequently  follows  an  emotional  shock  or  a  prolonged 
mental  strain,  whereas  traumatism,  as  in  railway  accidents,  is 
equally  liable  to  cause  functional  or  organic  disease. 

There  are  two  classes  of  signs  and  symptoms  which  point 
to  functional  rather  than  to  organic  disease — firstly,  the  absence 
of  characteristic  signs  of  organic  disease,  and  secondly,  the 
presence    of    certain    phenomena    peculiar   to   functional    disease. 


PARALYSIS   OF    UPPER   NEURONE    TYPE 


211 


Muscular  atrophy,  while  much  less  frequent  in  functional  than 
in  organic  palsies,  is  not  pathognomonic  of  organic  disease. 
Thus  Fig.  208  (p.  380)  shows  a  case  of  hysterical  monoplegia 
with  extensive  muscular  atrophy,  a  rare  combination.  But 
the  electrical  reactions  of  degeneration  never  occur  in  functional 
paralysis.  Their  presence  signifies  undoubted  organic  disease, 
somewhere  in  the  spino-muscular  neurone.  Paralysis  of  a  single 
muscle  is  pathognomonic  of  organic  disease ;  it  never  occurs  in 
functional  paralysis,   which   affects    whole    muscle-groups    or,    to 


Fig.  90. — Case  of  left  hemiplegia,  showing  phenomenon  of  combined  flexion 
of  hip  and  trunk  on  attempting  to  sit  up  without  using  arms. 

speak  more  accurately,  whole  movements.  To  sum  up,  then, 
the  diagnosis  between  functional  and  organic  paralysis  is  easy  if 
the  organic  palsy  is  of  the  lower  motor  neurone  type.  It  is 
chiefly  when  the  organic  lesion  is  in  the  upper  or  cortico-spinal 
neurone  that  difficulty  is  liable  to  occur,  i.e.  in  cases  where  there 
is  little  or  no  muscular  atrophy,  and  where  the  electrical  re- 
actions are  normal.  In  such  cases  the  presence  or  absence  of 
other  hysterical  stigmata  is  of  great  value. 

A  valuable  sign  of  organic  as  contrasted  with  hysterical  hemi- 
plegia is  Babinski's  combined  flexion  of  the  hip  and  trunk,  a 
phenomenon  almost  invariably  present  in  organic  cases.  To  elicit 
this  the  patient  lies  flat  on  his  back  on  a  smooth  hard  surface,  such 


212  NERVOUS    DISEASES 

as  a  table  or  the  floor,  with  his  arms  crossed  in  front  of  his  chest 
and  the  legs  not  allowed  to  touch  each  other.  We  then  ask  him 
to  sit  up  without  using  his  arms.  (See  Fig.  90.)  As  he  does  so,  the 
organically  paralysed  lower  limb  becomes  flexed  at  the  hip  and  the 
heel  is  raised  from  the  surface.  Meanwhile  the  shoulder  on  the 
healthy  side  is  carried  forwards,  as  if  to  counterpoise  the  contra- 
lateral lower  limb.  In  hysterical  hemiplegia  this  sign  is  absent,  and 
the  hysterically  paralysed  limb  remains  unraised.  Another  useful 
test  to  distinguish  between  organic  and  functional  paralysis  is  the 
fhenomenon  of  Grasset  and  Gaussel,^  which  is  also  confined  to 
organic  cases.  This  consists  in  inability  on  the  part  of  the  organically 
hemiplegic  patient  to  raise  both  lower  limbs  simultaneously  from  the 
surface  when  lying  down  as  before,  although  he  is  still  able  to  lift 
either  lower  limb  separately.  The  reason  for  this  peculiarity  is  that 
in  organic  hemiplegia  the  patient,  when  he  tries  to  lift  both  lower 
limbs  at  once,  is  unable  to  fix  the  pelvis.  In  testing  for  this  sign, 
we  must  be  careful  to  see  that  the  two  legs  do  not  touch  each 
other,  since  the  patient  often  tends  involuntarily  to  help  up  the 
paralysed  limb  by  means  of  the  sound  one.  Of  course,  the  sign  is 
only  present  in  cases  of  incomplete  hemiplegia.  Another  way  of 
showing  the  same  phenomenon  is  to  direct  the  patient  to  raise  the 
lower  limb  of  the  paralysed  side  and  hold  it  in  the  air.  If  we  now 
grasp  the  sound  leg  and  raise  it  up,  the  other  limb  at  once  falls 
down  again,  because  the  pelvis  cannot  be  steadied  by  the  muscles 
on  the  paralysed  side.  On  the  other  hand,  if  the  patient  first 
raises  the  sound  leg  and  we  then  passively  lift  the  paralysed  one, 
the  sound  limb  still  remains  in  the  air,  the  pelvis  remaining  fixed  by 
the  non-paralysed  muscles  of  the  healthy  side.  In  hysteria  there 
is  no  such  difference  between  the  separate  and  the  simultaneous 
raising  of  the  legs. 

In  some  cases  of  spastic  paraplegia  the  rigidity  of  the  lower 
limbs  is  of  diagnostic  value.  Thus  when  we  passively  hft  one 
lower  limb  off  the  bed  and  find  that  the  other  lower  Hmb  is 
thereby  lifted  up  as  well,  we  may  be  practically  certain  that  the 
rigidity  and  paralysis  are  organic  and  not  functional. 

1  Revue  neurologiquc,  1905,  p.  881. 


PARALYSIS    OF    UPPER    NEURONE    TYPE        213 

A  careful  study  of  the  reflexes  is  also  of  the  utmost  importance. 
The  presence  of  an  extensor  plantar  reflex  in  a  patient  beyond 
the  age  of  infancy  is  pathognomonic  of  organic  disease  (see  later, 
p.  319),  The  deep  reflexes,  whilst  they  may  be  exaggerated 
both  in  functional  and  in  organic  paralysis,  are  usually  normal 
in  functional  cases.  True  ankle-clonus  of  organic  disease  is 
generally  readily  distinguished  from  the  "  pseudo-clonus "  of 
functional  disease.  Absence  of  the  deep  reflexes  may  occur  in 
organic,  never  in  functional  disease. 

Incontinence  of  the  bladder  and  rectum  is  not  uncommon  in 
organic  diseases  of  the  spinal  cord  and  brain,  but  practically  never 
occurs  in  functional  paraplegia. 

Where  is  the  Organic  Lesion? — Suppose  we  have  come  to 
the  conclusion  that  the  patient's  motor  paralysis  is  organic  in  type, 
we  have  to  ask  ourselves  at  what  point  in  the  motor  path  the 
lesion  is  situated.  First,  we  must  decide  whether  the  lesion  is  in 
the  upper  (cortico-spinal),  or  in  the  lower  (nucleo-muscular)  motor 
neurone.  The  distinctive  characters  of  these  two  types  are  as 
follows  : — 

OEaANIC   MOTOR  PARALYSIS. 

Upper  (cortico-spinal)  Neurone.        Lower  (spino-muscular)  Neurone. 
Supra-Nuclear  Paralysis.  Nuclear    and    Infra -Nuclear 

Paralysis. 

1.  Diffuse     muscle-groups      affected,      1.  Individual  muscles  may  beaffected. 

never  individual  muscles. 

2.  Spasticity   and   hyper-tonicity   of      2.  Flaccidity  and  atonicity  of  para- 

paralysed  muscles.  lysed  muscles. 

3.  Alay  have  superadded  "  associated      3.  No  "  associated  movements." 

movements  "  on  attempted  vol- 
untary movement. 

4.  No  muscular  atrophy,  except  from      4.  Atrophy  of  paralysed  muscles. 

disuse. 

5.  Electrical  reactions  normal.  5.  Reactions  of  degeneration. 

6.  Deep  reflexes  in  paralysed  limbs      6.  Deep  reflexes  of  paralysed  muscles 

present,  and  usually  increased.  diminished,  and  often  absent. 

7.  If  foot  affected,  plantar  reflex  ex-      7.  Plantar   reflex,   if    present,    is   of 

tensor  in  type.  normal     flexor     type     (unless 

flexors   of  toes  are  themselves 
paralysed). 

Let  us  consider  some  of  these  points  more  in  detail.     Paralysis 

due  to  an  upper  neurone  lesion  never  af!ects  an  individual  muscle, 


214  NERVOUS    DISEASES 

but  always  a  diffuse  muscular  group.  The  converse,  however,  is 
not  true,  and  we  must  remember  that  even  a  lower  neurone  lesion 
may  produce  a  diffuse  paralysis,  where  a  series  of  adjacent  nerves 
or  nuclei  are  affected.  But  if  individual  muscles  are  picked 
out  by  paralysis,  the  adjoining  or  intermingled  muscles  being 
perfectly  normal,  the  cause  is  certainly  a  nuclear  or  infra-nuclear 
lesion. 

.Paralysis  frcm  a  cortico -spinal  lesion  is  rarely  permanently 
complete.  It  is  more  often  a  paresis  than  an  absolute  paralysis. 
In  this  respect  it  differs  from  the  total  palsy  of  a  spino-muscular 
lesion. 

Spasticity  of  the  paralysed  nmscles  in  supra-nuclear  lesions 
does  not  set  in  immediately  after  the  onset  of  a  sudden  lesion, 
but  usually  develops  gradually  in  the  course  of  from  one  to 
three  months.  Thus  in  a  typical  supra-nuclear  lesion,  as,  for 
example,  in  apoplexy,  there  is  an  initial  period  of  flaccidity, 
gradually  replaced  by  the  so-called  "  late  rigidity."  The  degree 
of  this  spasticity  varies  in  different  cases.  We  estimate  it  by 
moving  the  patient's  joints  passively,  and  comparmg  their  resistance 
with  that  of  a  healthy  limb. 

Patients  with  motor  paresis  due  to  cortico-spinal  lesions  not 
uncommonly  show  superadded  "  associated  movements "  on 
attempting  to  execute  a  voluntary  movement  with  the  paresed 
limb.  Thus,  for  example,  if  the  patient  tries  to  draw  up  his 
hemiplegic  leg,  he  cannot  do  so  without  at  the  same  time  dorsi- 
fiexing  the  ankle  involuntarily.  This  is  the  so-called  "  tibialis 
phenomenon  "  of  Striimpell.  Similarly  in  the  upper  limb  we  may 
note  an  analogous  "  pronation  phenomenon,"  consisting  of  a 
forced  pronation  on  attempting  to  flex  the  elbow. 

In  an  upper  neurone  lesion,  the  muscles  of  the  paralysed  limb, 
in  the  vast  majority  of  cases,  undergo  no  appreciable  atrophy, 
save  perhaps  to  a  very  slight  degree  from  disuse.  But  there 
are  occasional  exceptions  to  this  rule,  as  in  some  cases  of 
hemiplegia  which  are  associated  with  muscular  atroj^hy,  chiefly  in 
the  region  of  the  shoulder  or  in  the  intrinsic  muscles  of  the  hand. 
Such  atrophies  are  often  (but  not  always)  secondary  to  arthritic 


PARALYSIS    OF    UPPER    NEURONE    TYPE        215 

changes  in  the  joints.  But  however  intense  the  amyotrophy  of 
hemiplegia  may  be,  the  electrical  reactions  of  degeneration  are 
never  present.  Degenerative  reactions  (commonly  referred  to  as 
"  R.D.")  are  pathognomonic  of  a  nuclear  or  infra-nuclear  lesion. 
Not  that  R.D.  are  necessarily  present  in  every  lower  neurone 
lesion,  for  a  slight  lesion  of  a  nerve-trunk  may  produce  muscular 
palsy  without  R.D.,  and  in  many  nuclear  lesions,  for  example 
in  progressive  muscular  atrophy,  the  reactions  in  the  affected 
muscles  are  mixed,  owing  to  the  fact  that  degenerated  and 
healthy  muscle-iibres  are  intermingled  in  the  same  muscle,  the 
former  giving  R.D.,  the  latter  being  normal  in  reaction.  -  Again, 
in  the  motor  weakness  occurring  in  the  different  varieties  of 
myopathy,  there  is  simple  dimiimtion  both  to  faradism  and 
galvanism,  but  no  true  R.D.,  even  in  the  most  advanced  cases. 
The  reflexes  in  upper  and  lower  neurone  lesions  will  be  dealt  with 
more  fully  in  a  later  chapter  (p.  316). 

With  reference  to  the  differential  diagnosis  between  an  upper 
and  a  lower  neurone  lesion,  it  will  be  observed  that  no  single  sign 
of  the  six  we  have  mentioned  is  pathognomonic,  yet  the  sum  of  the 
various  points  usually  enables  us  without  difficulty  to  settle  with 
which  of  the  two  neurones  we  have  to  deal.  Sometimes  there  is  a 
combined  lesion  of  upper  and  lower  neurones,  as  in  a  transverse 
myelitis  or  a  myelomalacia.  Here  the  phenomena  at  the  level  of 
the  lesion  will  be  of  a  flaccid,  lower  neurone  type,  due  to  destruc- 
tion of  the  anterior  cornua  and  anterior  roots,  whilst  below  that 
level  there  is  a  spastic  paraplegia  of  cortico-spinal  type,  from 
interruption  of  the  pyramidal  tracts. 

Motor  Palsies  of  Upper  Neurone  Type. — The  signs  and 
symptoms  vary  according  to  the  level  at  which  the  cortico- 
spinal tract  is  damaged.  The  following  are  the  chief  sites  at 
which  a  lesion  may  occur,  and  the  diagnostic  signs  of  each 
(see  Fig.  6,  p.  7). 

A  cortical  lesion  in  the  pre-central  convolution  is  often 
locahsed  to  a  single  limb  and  is  more  hkely  to  produce  a  mono- 
plegia than  a  hemiplegia,  since  only  a  very  extensive  cortical 
lesion  would  produce  a  complete  hemiplegia,  affecting  face,  arm 


216  NERVOUS   DISEASES 

and  leg.  What  we  usually  find  is  either  a  pure  monoplegia — crural, 
brachial,  or  facial,  or,  if  the  lesion  be  somewhat  larger,  an  associ- 
ated monoplegia — brachio- crural,  or  facio -brachial.  Cortical  motor 
paralysis  is  commonly  associated  with  local  epileptiform  attacks  of 
the  paralysed  limb,  because  disease  may  irritate  the  cortex  in 
addition  to  paralysing  it.  The  monoplegic  limb  frequently  shows 
a  cortical  type  of  anaesthesia,  which,  as  we  have  already  seen,  is 
slight  in  degree,  more  marked  at  the  periphery  of  the  limb,  and 
often  transient  in  duration. 

A  strictly  localised  subcortical  lesion  is  often  indistinguishable 
from  a  cortical  one,  save  by  the  absence  of  irritative  epileptiform 
phenomena ;  and  in  many  cases  the  lesion  is  both  cortical  and 
subcortical. 

A  lesion  in  the  motor  path  at  the  level  of  the  internal  capsule, 
inasmuch  as  all  the  pyramidal  fibres  have  by  this  time  converged 
to  form  a  compact  strand,  produces  no  longer  a  monoplegia  but  a 
complete  hemiplegia,  affecting  face,  arm  and  leg.  There  are  no 
Jacksonian  convulsions  as  in  a  cortical  lesion.  If  the  capsular 
lesion  extends  backwards  from  the  motor  into  the  sensory  tract,  or 
into  the  optic  thalamus,  there  may  be  a  coexistent  hemi-anaesthesia, 
but  this  is  not  common. 

A  thalamic  lesion  is  sometimes  associated  with  hemi-athetosis 
of  the  hemiplegic  side  ;  this  athetosis  does  not  appear  immediately 
after  an  attack  of  apoplexy,  but  develops  gradually  in  the  coarse 
of  many  weeks.  A  still  more  extensive  lesion,  extending  back- 
wards along  the  capsule  from  the  motor  tract,  through  the  sensory 
path  and  into  the  optic  radiations,  will  cause  hemiplegia,  hemi- 
ansesthesia  and  hemianopia. 

In  rare  cases  we  may  have  an  ipso-latercd  hemi2olegia  in 
which,  for  example,  a  lesion  of  the  left  cerebral  hemisphere  pro- 
duces a  left-sided  hemiplegia.  Some  of  these  cases,  according  to 
Marie,  are  due  to  congenital  non-decussation  of  the  pyramids  ; 
others  result  from  a  dural  hsematoma,  a  meningeal  haemorrhage 
or  a  superficially  situated  tumour,  whereby  the  contra-lateral 
pyramidal  tract  is  compressed  against  the  base  of  the  skull. 
From  the  surgical  point  of  view  we  must  also  bear  in  mind  the 


PARALYSIS    OF    UPPER    NEURONE    TYPE        217 

occasional  occuiTence  of  a  false  ijJ so-lateral  hemiplegia  where  a 
blow  on  one  side  of  tlie  head,  say  the  left,  is  followed  by  a  left- 
sided  hemiplegia.  Such  cases  are  generally  due  to  injury  of  the 
opposite  {i.e.  the  right)  hemisphere  by  "  contre-coup." 

A  lesion  in  the  crus  cerebri  is  recognised  by  the  coexistence 
of  third  nerve  palsy  on  one  side,  with  hemiplegia  of  the  opposite 


Fig.  91. — Lesion  of  left  crus  cerebri — "  Weber's  syndrome."  Patient  is 
looking  upwards  and  attempting  to  show  the  teeth  on  both  sides. 
There  is  dilatation  of  the  left  pupil  and  paralysis  of  the  left  superior 
rectus,  together  with  hemiplegia  of  the  riyht  face,  arm  and  leg. 

face,  arm  and  leg,  usually  most  marked  in  the  face.  This  variety 
of  alternate  paralysis  is  known  as  Weber^s  syndrome  (see  Fig.  91). 
The  third  nerve  palsy  is  often  incomplete.  When  the  lesion 
extends  into  the  tegmentum  and  imphcates  the  neighbourhood  of 
the  red  nucleus,  it  may  produce  a  unilateral  tremor  or  a  hemi- 
ataxy  of  the  hemiplegic  side,  combined,  as  before,  with  a  third 
nerve  affection  on  the  side  of  the  brain  lesion ;  this  combination 
is  known  as  Benedikt's  syndrome.  If  the  lesion  extends  outwards 
so  as  to  impHcate  the  optic  tract  as  it  winds  round  the  outer  side 
of  the  crus,  there  may  be  superadded  a  hemianopia. 

As  we  come  downwards  along  the   pyramidal  tract  into  the 


218  NERVOUS    DISP^ASES 

pons  and  medulla,  the  type  of  hemiplegia  changes ;  there  is  no 
longer  third  nerve  palsy,  but  on  reaching  the  level  of  the  facial 
nerve,  another  variety  of  alternate  hemiplegia  appears.  This 
consists  of  facial  palsy,  peripheral  in  type,  on  the  side  of  the  lesion, 
together  with  hemiplegia  of  the  arm  and  leg  on  the  opposite  side, 
the  so-called  Millard-Gubler  syndrome.  Other  cranial  nerves  on  the 
side  of  the  pontine  or  bulbar  lesion,  for  example,  the  trigeminal, 
the  sixth,  or  the  hypoglossal,  may  be  afiected  together  with 
the  pyramidal  tract,  and,  as  in  the  Millard-Gubler  syndrome, 
may  co-exist  with  hemiplegia  of  the  opposite  arm  and  leg,  but 
such  cases  are  rare.  As  they  descend  through  the  medulla  the 
pyramidal  tracts  of  opposite  sides  converge  and  eventually  lie 
so  close  together  that  at  this  level  a  strictly  unilateral  lesion 
seldom  occurs,  there  being  usually  damage  to  both  pyramidal 
tracts  affecting  the  limbs  of  both  sides,  though  perhaps  in  unequal 
degree.  And  together  with  this,  there  are  "  bulbar  "  symptoms 
— disorders  of  articulation,  phonation,  or  deglutition,  from  impli- 
cation of  the  tenth,  eleventh  and  twelfth  cranial  nerves  or  nuclei. 

The  diagnosis  of  motor  paralysis  due  to  lesions  of  the  pyramidal 
tract  within  the  cord  depends  on  the  level  of  the  lesion.  The 
two  pyramidal  tracts  decussate  at  the  lower  end  of  the  medulla 
oblongata,  so  that  a  unilateral  lesion  of  the  spinal  cord  pro- 
duces an  ipso -lateral  instead  of  a  contra-lateral  motor  paralysis. 
If  the  lesion  be  in  the  cervical  region,  the  arm  and  leg  on  the 
corresponding  side  will  be  affected;  but  if  it  be  situated  below 
the  cervical  enlargement,  the  leg  on  the  side  of  the  lesion  suffers 
alone.  A  primary  unilateral  lesion  of  the  cord  generally  interrupts 
not  only  motor  but  sensory  paths,  and  produces  the  well-known 
Brown-Sequard  paralysis,  to  which  reference  has  already  been 
made. 

Bilateral  motor  paralysis  of  upper  neurone  type  is  due  to  bi- 
lateral lesions,  which  may  be  situated  either  in  the  brain  or  in  the 
spinal  cord.  When  both  pjTamidal  tracts  are  affected  within  the 
brain  (and  the  commonest  cause  is  a  double  focus  of  softening,  in 
the  region  of  the  posterior  part  of  the  lenticular  nucleus,  though 
less  commonly  the  lesions  are  cortical  or    subcortical)    a  double 


PARALYSIS    OF    UPPER    NEURONE    TYPE        219 

hemiplegia  is  the  result.  In  these  cases  of  double-hemiplegia  or 
diplegia  there  are,  besides  the  signs  of  hemiplegia  on  both  sides 
(frequently  unequal  in  degree),  what  are  known  as  "  pseudo-bulbar  " 
phenomena.  In  pseudo-bulbar  paralysis,  the  symptoms  of  which  we 
have  already  studied  (p.  113),  it  is  uncommon  for  the  two  attacks 
of  hemiplegia  to  occur  simultaneously  on  the  two  sides  ;  they  more 
usually  occur  successively,  and  it  is  only  after  the  hemiplegia  has 
bee: me  bilateral  that  the  pseudo-bulbar  symptoms  appear.  Such 
patients  are  generally  excessively  emotional,  tending  on  slight 
provocation  to  laugh  or,  more  frequently,  to  weep  with  a  pecuhar 
"  spastic "  wail,  and  an  unnatural  slowness  of  expressional 
movement. 

Bilateral  pyramidal  lesions  within  the  spinal  cord  produce  para- 
plegia, affecting  all  four  limbs  if  the  lesion  be  above  the  cervical 
enlargement,  but  affecting  the  lower  Hmbs  alone  if  the  lesion  be 
below  the  cervical  region ;  it  is  commonly  of  the  ordinary 
spastic  type,  with  increased  deep  reflexes.  If  the  sensory 
tracts  be  interrupted  by  the  same  lesion  as  that  which  has  affected 
the  motor  tracts,  we  have  superadded  an  anaesthesia  whose  upper 
limit  corresponds  to  that  of  the  highest  affected  segment. 
Such  cases  of  combined  sensory  and  motor  paralysis  usually  have 
loss  of  control  of  the  sphincters.  If  the  cord  lesion  be  sufficiently 
extensive  to  implicate  the  anterior  cornua,  there  will  be  muscular 
atrophy,  locahsed  to  the  segment  affected,  i.e.  at  the  upper 
boundary  of  the  spastic  paraplegia.  But  it  is  important  to 
remember  that  if  the  lesion  of  the  cord  be  one  which  completely 
divides  it  [e.g.  a  stab  or  bullet-wound),  so  that  there  is  no  con- 
nection between  the  cord-segments  above  and  below  the  lesion, 
the  paraplegia  is  then  flaccid  in  type  and  the  deep  reflexes  are 
absent  in  the  paralysed  limbs.  The  plantar  reflexes,  however, 
persist  and  are  of  the  extensor  type,  be  the  lesion  complete  or 
incomplete. 

The  differential  diagnosis  between  tumours  arising  within  the 
spinal  cord  and  those  growing  from  without,  is  sometimes 
difficult.  In  extra-medullary  tumours,  arising  from  the 
nerve-roots  or  meninges   on    the    posterior  aspect    of    the   cord. 


220  NERVOUS    DISEASES 

root-pains,  unilateral  or  bilateral,  usually  precede  the  signs  of 
transverse  cord  lesion,  viz.,  paraplegia  with  affection  of  sensa- 
tion, increased  deep  reflexes,  &c.  But  if  the  extra-medullary 
growth  starts  in  front  of  the  cord,  root-pains  are  absent  or  late. 
If  the  anterior  roots  be  involved,  muscular  atrophy  of  root  dis- 
tribution is  a  valuable  focal  sign.  Spontaneous  reflex  spasms 
of  the  lower  limbs  are  commoner  in  extra-medullary  than  in 
intra-medullary  growths.  An  extra-medullary  tumour  situated 
laterally  sometimes  compresses  the  cord  so  as  to  produce  an 
incomplete  Brown-Sequard  syndrome.  Thus  in  one  case  of  my 
own,  where  an  endothelioma  was  removed  from  the  first  thoracic 
root  on  the  right  side,  the  patient  had  asymmetrical  spastic 
paraplegia,  more  marked  in  the  right  leg,  together  with  impair- 
ment of  thermal  and  pain  sense  in  the  left  leg  and  left  side  of  the 
trunk. 

The  tendency  is  to  localise  a  spinal  tumour  below  its  actual 
level.  Sometimes  valuable  indications  are  provided  by  studying 
the  vibration  sense  of  the  vertebral  spines,  this  sensibility  often 
being  lost  up  to  the  level  of  the  growth. 

Sometimes  a  diagnosis  of  extra-medullary  tumour  is  made, 
and  operation  or  autopsy  shows  the  condition  to  be  one,  not  of 
tumour  but  of  localised  subacute  or  chronic  lepto-meningitis. 
This  mistake  may  sometimes  be  avoided  by  studying  the  exact 
distribution  of  the  initial  root-pain.  In  tumour  this  pain  is 
localised  to  a  single  root  at  the  start ;  in  meningitis  the  pain  is 
more  diffuse,  affecting  a  considerable  number  of  root-areas. 

Sometimes  the  lesion  is  not  horizontal,  but  higher  on  one  side 
than  the  other,  and  then  the  upper  hmit  of  the  anaesthesia  will  be 
correspondingly  uneven  on  the  two  sides,  and  the  distribution  of 
muscular  atrophy  from  anterior  cornual  destruction  correspond- 
ingly asymmetrical. 

We  also  meet  with  cases  of  bilateral  spastic  paraplegia  without 
any  affection  of  sensation.  Such  cases  may  be  examples  of 
slowly  progressive  primary  lateral  sclerosis,  a  rare  disease,  or  what 
is  more  usual,  of  amyotrophic  lateral  sclerosis,  where  the  signs  of 
a    progressive  muscular  atrophy  are  superadded  to  rigidity  of  the 


PARALYSIS    OF    UPPER    NEURONE    TYPE        221 

lower  limbs  with  increased  deep  reflexes.  A  pure  motor  paraplegia 
is  more  frequently  due  to  disseminated  sclerosis,  to  an  imper- 
fectly recovered  transverse  myelitis,  or  to  some  other  vascular 
lesion,  as  thrombosis  or  haemorrhage,  in  which  the  sensory  func- 
tions have  subsequently  become  restored,  the  motor  tracts  re- 
maining permanently  sclerosed.  The  history  of  the  case  is 
sufficient  to  distinguish  these  diseases. 

Syringomyelia,  when  it  affects  the  pyramidal  tracts,  may  also 
produce  a  spastic  type  of  paraplegia ;  but  it  is  readily  recognised 
by  the  accompanying  characteristic  dissociated  anaesthesia,  to 
which  we  have  already  referred  (p.  202),  and  frequently  by  the 
coexistence  of  atrophic  changes  in  the  bones,  joints  and  muscles, 
muscular  atrophy  occurring  when  the  anterior  cornua  are  implicated 
in  the  gliomatous  process. 


CHAPTER   Xiy 

ORGANIC   MOTOR   PARALYSIS   OF   LOWER  NEURONE   TYPE 

Motor  Palsies  of  Lower  Neurone  Type. — Here,  as  in  upper 
neurone  lesions,  the  signs  and  symptoms  differ  according  to  the 
level  at  which  the  spino-muscular  neurone  is  diseased.  The  most 
important  diagnostic  fact,  for  localising  purposes,  is  the  presence 
or  absence  of  sensory  phenomena.  If,  in  a  lower  neurone  motor 
palsy,  sensory  changes  are  present,  we  have  to  do  with  a  lesion 
of  a  mixed  nerve,  that  is,  of  a  nerve  containing  sensory  as  well 
as  motor  fibres.  If,  on  the  other  hand,  sensory  changes  are  absent 
throughout  the  course  of  the  disease,  the  spino-muscular  neurone 
is  probably  affected,  either  before  it  is  joined  by  the  sensory  fibres 
{i.e.  the  lesion  is  in  the  anterior  cornu  or  anterior  nerve-root),  or 
after  it  has  parted  company  with  them  {i.e.  the  lesion  is  in  a 
purely  motor  nerve-branch  or  in  the  muscle  itself). 

A  lesion  of  the  anterior  cornu  within  the  cord  (as  of  its  homo- 
logue  in  the  motor  nuclei  of  the  bulb)  is  unassociated  with  any 
sensory  paralysis,  and  therefore  produces  a  pure  motor  palsy  of 
the  corresponding  muscle  fibres.  A  lesion  of  the  anterior  nerve-root, 
emerging  from  the  anterior  cornu,  produces  identical  signs,  and  is 
often  indistinguishable  from  an  intra-spinal  nuclear  lesion.  In 
nuclear  or  anterior-root  lesions,  therefore,  we  find  pure  motor  palsy, 
of  lower  neurone  type,  unassociated  with  any  sensory  change.  The 
commonest  examples  of  such  lesions  are  chronic  anterior  polio- 
myelitis (progressive  muscular  atrophy)  and  certain  types  of  lead 
paralysis.  Acute  anterior  polio-myelitis  (infantile  paralysis  of 
spinal  type)  in  the  early  days  or  weeks  of  the  disease  is  frequently 
associated  with  pain  and  tenderness  of  the  limbs.  As  the  malady 
subsides  into  the  chronic  stage,  the  pain  and  tenderness  pass  of!. 
Landry's  paralysis  is  a  pure  motor  paralysis  of  the  whole  spino- 
muscular  neurone,  to  which  we  shall  refer  presently.     A  nuclear  or 


PARALYSIS    OF    LOWER    NEURONE    TYPE        223 


anterior  root  lesion  is  further  characterised  by  the  "  root "  dis- 
tribution of  the  motor  paralysis,  so  that  in  this  respect  it  differs 
from  the  paralysis  due  to  a  lesion  of  a  peripheral  nerve  (see  Tables 
of  Root  Distribution,  p.  34).  Lesions  of  peripheral  mixed  nerves 
are  always  associated,  at  the  onset  at  least,  with  sensory  changes. 
In  the  case  of  lesions  of  peripheral 
purely  motor  nerves  {e.g.  the  nerve  of 
Bell  to  the  serratus  magnus),  the 
distribution  of  the  motor  palsy  is 
totally  unlike  that  of  a  nuclear  or 
anterior  root  lesion. 

To  distinguish  between  a  nuclear 
and  an  anterior  root  lesion  is  some- 
times difficult,  and  may  in  some 
instances  be  impossible.  The  co- 
existence of  spastic  phenomena  corre- 
sponding to  lower  parts  of  the  cord 
points  to  an  intra-spinal  lesion,  and 
indicates  a  co-existing  lesion  of 
the  adjacent  pyramidal  tract.  Total 
escape  of  the  pyramidal  tract,  on  the 
other  hand,  would  suggest  an  anterior 
root  lesion,  though  not  necessarily  so, 
since  acute  anterior  polio -myelitis  does 
not  affect  the  pyi'amidal  tract.  An- 
other point  which  may  sometimes  help 
us  is  the  subsequent  course  of  the 
disease ;  if  the  paralysed  muscles 
recover,  this  is  in  favour  of  an  extra-  medullary  anterior  root  lesion 
rather  than  an  affection  of  the  anterior  cornu,  inasmuch  as 
regeneration  of  nerve- fibres  only  occurs  in  extra-spinal  lesions,  an 
intra-spinal  lesion  of  the  grey  matter  being  irreparable. 

A  pure  anterior  cornual  lesion,  with  its  absence  of  cutaneous 
anaesthesia,  can  only  be  confounded  with  a  lesion  either  in  a  purely 
motor  nerve,  or  with  one  in  the  muscle-fibres  themselves.  The 
history  of  the  onset  of  the  disease  is  of  great  importance,  so  also 


Fig.  92.  —  Old  acute  autenor 
polio-myelitis,  with  atrophy 
of  deltoid  and  biceps,  and 
deficient  growth  of  the 
humerus  on  the  left  side. 


224 


NERVOUS    DISEASES 


is  the  exact  distribution  of  the  muscular  paralysis.  The  two  chief 
diseases  specially  affecting  the  anterior  cornua  are  infantile 
paralysis  and  progressive  muscular  atrophy.  Acute  anterior  polio- 
myelitis  or  infantile  spinal  paralysis  is  really  a  constitutional 
disease  due  to  an  infective  virus.  It  has  a  sudden  onset, 
generally  febrile.  The  virus,  whilst  causing  congestion  of  various 
organs,  including  the  spleen  and  lymphatic  glands,  has  a  specially 
intense  effect  upon  the  central  nervous   system  and  produces  a 

special  perivascular  infiltration 
around  the  anterior  spinal  ar- 
teries, which  supply  the  anterior 
horns.  The  spinal  meninges  are 
also  hyperaemic,  hence  there  are 
pains  in  the  limbs,  aggravated 
by  passive  movement.  A  large 
number  of  muscles,  sometimes  in 
all  four  limbs,  may  be  paralysed 
at  the  beginning.  But  in  a  week 
or  so  most  of  the  paralysis  clears 
up,  leaving  a  residuum,  almost 
always  unilateral,  of  paralysed 
muscles  which  undergo  rapid 
wasting.  There  is  no  exaggera- 
tion of  tendon  reflexes  below  the 
level  of  the  lesion,  since  the  pyra- 
midal tract  is  unaffected.  Eigs. 
92,  93,  and  94  are  examples  of  cases  of  old  infantile  paralysis, 
showing  the  extreme  degree  of  atrophy  which  results,  and  if 
the  disease  occurs  in  childhood,  as  is  most  often  the  case,  the 
subsequent  want  of  growth  in  the  limb.  The  wasted  limb  is 
often  cold  and  blue,  and  the  patient  can  frequently  tolerate, 
without  pain,  faradic  stimulation  of  a  strength  which  is  intolerable 
in  the  sound  limbs. 

Chronic  anterior  polio -myelitis,  or  progressive  muscular  atrophy, 
has  a  gradual,  insidious  onset.  It  occurs  almost  always  in  adults 
and,  though  beginning  unilaterally,   generally  becomes  bilateral. 


Fia.  93. — Old  iufantile  paralysis  with 
total  loss  of  deltoid  and  biceps. 
Shows  action  of  the  supinator 
longus   in  flexion  of  elbow. 


PAEALYSIS    OF    LOWER    NEURONE    TYPE         225 


It  usually  shows  itself  first  in  the  small  intrinsic  muscles 
of  the  hands  (Fig.  95)  ;  more  rarely  it  begins  in  the  shoulder 
muscles.  In  this  disease  we  observe  fibrillary  worm-like  tremors 
in  the  wasting  muscles,  whose  electrical  reactions  are  a  mixture  of 
R.D.  with  healthy  reactions.  This  is  because  here  and  there  in 
the  diseased  area  a  healthy 
anterior  cornual  cell  survives, 
together  with  its  correspond- 
ing healthy  muscle-fibre.  If 
the  adjacent  pyramidal  tracts 
be  sclerosed,  we  have  amyo- 
trophic lateral  sclerosis,  in 
which  the  deep  reflexes  are 
exaggerated  and  the  plantar 
reflexes  extensor  in  type. 

There  is  a  rare  infan- 
tile variety  of  progressive 
muscular  atrophy — We:'dn{g- 
Hoffmann  type — due  to  de- 
generation of  the  anterior 
cornua.  The  disease  begins 
in  infancy,  often  during  the 
first  few  months  after  birth. 
The  muscles  of  the  lower 
limbs  are  attacked  first,  pro- 
ducing weakness  and  wasting, 
though  the  atrophy  may  be 
masked  by  subcutaneous  fat.  The  knee-jerks  disappear  and  the 
atrophied  muscles  lose  their  electrical  excitability.  The  disease 
gradually  spreads  upwards  to  the  medulla  and  is  fatal,  with  bulbar 
symptoms,  in  from  one  to  six  years. 

There  is  another  pecuhar  form  of  muscular  atrophy  which  is 
hereditary  and  runs  in  families,  known  from  its  distribution  as 
Tooth's  "  peroneal  "  t3rpe,  or  as  the  progressive  neuritic  amyotrophy  of 
Charcot  and  Marie.  It  comes  on  in  childhood,  commencing  in  the 
distal  muscles  of  the  hmbs,  more  often  the  lower  limbs  and  the 


Fig.  94. — Old  infantile  paralysis  (acute 
anterior  polio-myelitis).  Paralysis  and 
atrophy  of  all  the  muscles  below  the 
elbow,  with  exception  of  supinator 
lona;us. 


226 


NERVOUS    DISEASES 


peroneal  muscles,  and-  gradually  producing  weakness  with  con- 
tractures. Talipes  equino-varus  appears,  for  whicli  tenotomy  is 
often  done,  as  was  tlie  case  in  the  patient  shown  in  Fig.  96. 
But  if  the  patient's  feet  be  passively  supported,  say  by  metal 
supports  at  the  ankles,  until  the  paralysis  of  the  limbs  has  become 
complete  (as  in  the  patient  shown  in  Fig.  98),  talipes  does  not 
appear  even  in  the  totally  paralysed 
limb.  Later,  the  intrinsic  muscles  of 
the  hands  undergo  wasting  (Fig.  98). 
In  fact,  early  claw-foot  and  claw-hand 
in  young  people  are  almost  pathogno- 
monic. The  only  other  disease  of  diag- 
nostic importance  in  this  connection  is 
interstitial  hypertrophic  neuritis.  The 
disease  hardly  ever  extends  to  the 
muscles  of  the  hips  or  shoulders.  The 
facial  and  trunk  muscles  also  escape. 
It  is  interesting  to  note  that  when  'all 
the  muscles  below  the  knees  are  para- 
lysed, the  patient  may  still  be  able  to 
walk  alone,  though  the  gait  is  high- 
stepping  from  drop-foot.  This  was  so  in 
both  the  patients  here  figured.  The  deep 
reflexes  are  lost  in  the  atrophied  muscles. 
Thus  in  the  little  boy  (Fig.  96)  the  ankle- 
jerks  were  lost,  whilst  the  knee-jerks 
remained  brisk,  since  the  thigh  muscles 
were  unaffected  ;  in  the  girl  (Fig.  98)  the  knee-jerks  and  ankle- 
jerks  were  both  lost.  Pathologically  the  disease  is  associated  with 
atrophy  of  the  anterior  cornual  cells,  whilst  the  anterior  nerve- 
roots  are  said  to  be  healthy.^  But  there  is  marked  degeneration 
in  the  intra-muscular  nerve -fibres  of  the  affected  muscles.  There 
is  also  a  curious  degeneration  in  the  posterior  columns,  closely 
resembling  that  of  tabes  dorsalis. 

Hypertrophic   interstitial  neuritis  is   another    family    disease 


Fiy.  9J. — Progressive  mus- 
cular atrophy  in  a  man 
aged  32.  The  patient  was 
also  tabetic. 


'   Dejerine  and  Armand-Delille,  Revue  neurologique,  ]g03,  p.  Hf 


PARALYSIS  OF  LOWER  NEURONE  TYPE 


227 


which  begins  in  childhood  or  adolescence.  In  this  disease, 
besides  a  flaccid  muscular  atrophy  of  the  limbs,  commencing 
peripherally  and  less  intense  in  the  proximal  muscles,  there  are 
marked  sensory  changes,  resembling  those  of  tabes,  i.e.  shooting 
pains,  anaesthesia,   analgesia  (especially  at  the  periphery  of  the 


Fig.  96. 


Fig.  97. 


Figs.  96  and  97. — Peroneal  type  of  muscular  atrophy  (Charcot-Marie- 
Tooth).  In  spite  of  total  paralysis  below  the  knees,  the  patient  is 
still  able  to  stand  and  walk. 

limb),  loss  of  joint-sense,  &c.  There  is  marked  ataxia  of  the 
limbs  together  with  loss  of  the  deep  reflexes,  kypho-scoliosis,  and 
Argyll-Robertson  pupils.  In  some  cases  exophthalmos  has  been 
observed.^  Pathologically  we  find  a  sclerotic  thickening  of  the 
peripheral  nerve-trunks,  extreme  in  degree,  often  palpable  during 
life,  or  even  visible  if  the  patient  be  thin.  There  is  also  a 
degeneration   of   the  posterior  columns,    somewhat    like    that  of 

^  Boveri,  La  simaine  meclicale,  30th  March  1910,  p.  145. 


228 


NBKVOUS    DISEASES 


tabes    dorsalis.      The    muscles    show    atrophy,    proliferation    of 
sarcolemma  nuclei,   and  fatty  infiltration. 

A   lesion    of   a    spinal   nerve   after  the   union  of  its  anterior 
with  its   posterior   root,   but  above   the  point  where  it  divides 

into  branches  to  form  plexuses  or  in- 
dividual nerves,  is  characterised  by  a 
combination  of  motor  and  sensory 
paralysis,  the  distribution  of  which 
is  not  according  to  peripheral  nerves, 
but  according  to  root  areas,  motor 
and  sensory  (see  Tables  of  Muscular 
Localisation,  p.  34,  also  Fig.  20,  p.  35). 
Thus,  for  example.  Fig.  99  is  the 
photograph  of  a  sailor  who  received 
a-  violent  blow  on  the  right  side  of 
his  neck  from  an  iron  winch.  This 
produced  paralysis  of  the  deltoid, 
supra-  and  infra  -  spinatus,  biceps, 
brachialis  anticus,  and  supinatores 
longus  and  brevis,  together  with  an 
area  of  cutaneous  anaesthesia  along 
the  outer  side  of  the  whole  upper 
limb,  from  the  shoulder  to  the  hand. 
All  this  would  be  difficult  of  explana- 
tion on  the  theory  of  multiple  injuries 
to  the  numerous  peripheral  nerves 
which  supply  these  various  parts.  But 
the  motor  distribution  is  that  of  the 
fifth  cervical  root,  whilst  the  anaes- 
thesia of  the  hand  corresponds  to  the 
fifth  and  a  small  part  of  the  sixth  root,  and  as  a  matter  of  fact 
this  lesion  was  subsequently  verified  by  operation. 

Lesions  of  peripheral  mixed  nerves,  when  complete,  are  usually 
easy  of  diagnosis,  inasmuch  as  there  are  paralysis  and  atrophy  of 
all  the  muscles  supphed  by  the  particular  nerve,  together  with 
anesthesia  in  the  area  of  its  cutaneous  distribution.     It  is  un- 


FlG.  98.  —  Peroneal  type  of 
muscular  atrophy  (Charcot- 
Mftrie  -  Tooth).  Showing- 
atrophy  of  intrinsic  muscles 
of  hands. 


PARALYSIS    OF    LOWER    NEURONE    TYPE 


229 


necessary  to  discuss  the  signs  of  paralysis  of  all  the  various 
mixed  nerves.  The  question  is  one  of  anatomy.  Let  us 
select  one  or  two  illustrative  ex- 
amples. Ulnar  paralysis  af!ects 
certain  muscles  of  the  hand  and 
forearm,  of  which  the  most  im- 
portant diagnostically  are  the 
interossei  and  the  two  ulnar 
lumbricales.  Owing  to  paralysis 
of  the  interossei,  extension  of  the 
interphalangeal  joints  is  im- 
paired, especially  in  the  two 
ulnar  fingers  whose  lumbricales 
are  also  aflected.  Anaesthesia  of 
one  and  a  half  fingers  and  of  the 
corresponding  part  of  the  hand 
is  also  present  (see  Pigs.  100  and 
101,  which  are  taken  from  a  case 
where  the  nerve  was  cut  by  the 
bursting  of  a  soda-water  bottle). 
In  old-standing  cases,  the  unop- 
posed common  extensor  of  the 
fingers  undergoes  contracture  and 
produces  a  claw-hand,  this  for  the 
same  reason  being  most  evident 
in  the  two  ulnar  fingers.  The 
hypothenar  eminence  also  be- 
comes flattened  and  the  palm 
hollowed,  so  that  the  flexor  ten- 
dons become  visible  beneath  the 
skin. 

Figs.  102  and  103  are  from  a 
case  of  division  of  the  sciatic  nerve  from  a  bullet-wound  in  the 
thigh  in  a  young  soldier.  It  shows  how  all  the  muscles  below  the 
knee  are  atrophied  and  paralysed,  the  hamstring  muscles  having 
escaped,    since   the   nerve   was   divided    below  the  level    of   the 


FiGr.  99. — Case  of  rupture  of  (J5  root 
in  a  sailor  aged  29.  There  are 
atrophy  and  paralysis  of  deltoid, 
supra-  and  iufra-spinatus,  biceps, 
brachial  is  anticus,  and  supina- 
tores  longus  and  brevis,  to- 
gether with  anesthesia  along  the 
outer  side  of  the  limb,  from  the 
neck  to  the  thumb  and  index  (in 
the  area  indicated  by  black  line). 
The  figure  shows  the  atrophy  of 
the  deltoid  with  downward  dis- 
placement of  the  limb  at  the 
shoulder-joint. 


230 


NERVOUS    DISEASES 


hamstring  brandies.  Besides  the  muscular  atrophy  with  the 
usual  drop-foot,  we  have  anaesthesia  in  the  areas  of  the  peroneal, 
musculo-cutaneous,  anterior  tibial,  short  saphenous  and  both 
plantar  nerves. 

As   a   mixed   nerve   recovers,  sensation  returns   more   rapidly 


Fia.  100. 


Fig.  101. 


Figs.  100  and  101. — ^Ulnar  paralysis,  from  a  wound  of  the  nerve  behind 
the  internal  condyle  of  the  humerus.  The  area  within  the  black  line 
is  ansesthetic. 


than  motor  power,  and  protopathic  .sensation  earlier  than  epicritic. 
We  must  therefore  be  prepared  to  find  that  in  a  long-standing 
case  the  sensory  loss  is  less  complete  than  in  a  recent  one, 
or  it  may  happen  that  sensation  is  quite  restored  when  motor 
power  has  not  yet  returned.  This  rule,  however,  is  by  no  means 
invariable. 

As  an  example  of  paralysis  of  a  pure  motor  nerve,  we  may 


PARALYSIS    OF    LOWER    NEURONE    TYPE 


231 


select  the  posterior  thoracic,  or  nerve  of   Bell,  which  supplies  the 
serratus  magnus.     Fig.  104  is  from  such  a  case,  and  it  shows  the 


CO  ^ 

^  g 

o  c 
^^ 

o 

!>    to 

^  J 

9    m 

2.S 

'^  o 


(D  ii 

>  o 

tH      O 

«    !^ 
o  p 

to    -ti 


>!  o 


2     Pi 


characteristic  "  wiliging  "  of  the  scapula  when  the  patient  holds 
his  arms  horizontally  forwards. 

When  a  pure  motor  paralysis  of  lower  motor  neurone  type 


232  NERVOUS    DISEASES 

recovers,  tJiis  indicates  tliat  it  must  have  been  of  extra-medullary 
origin,  since  regeneration  of  nerve-fibres  does  not  occur  within  the 
central  nervous  system. 

Besides  such  lesions  of  individual  nerve-trunks,  we  have  also 
to  bear  in  mind  so-called  multiple  or  feripheral  neuritis — a  very 
common  disease,  affecting  the  mixed  nerves  symmetrically  on 
both  sides,  sometimes  in  the  arms,  sometimes  in  the  legs,  some- 
times in  all  four  limbs,  and  even  also  other  nerves  such  as  those  of 


Fig.  104. — Paralysis  of  serratus  magnus  on  right  side.  The  patient  is 
holding  both  arms  horizontally  forwards.  The  lower  fibres  of  the 
trapezius  are  also  paralysed. 

the  soft  palate,  diaphragm,  and  so  on.  Such  neuritis,  when  affecting 
mixed  nerves,  is  easy  of  diagnosis.  The  distribution  of  the  sensory 
and  motor  abnormalities  is  characteristic.  The  patient  has  subjec- 
tive tingling  feelings  in  the  hands  and  feet,  and  on  examination  we 
find  diminution  of  sensation  to  fight  touches  in  the  "  stocking  " 
and  "  glove  "  areas  of  the  limbs,  often  with  extreme  hypersesthesia 
of  the  soles  to  pressure.  Moreover,  the  muscles  of  the  limbs  are 
exquisitely  tender  on  being  grasped.  The  motor  paralysis,  of  the 
lower  motor  neurone  type,  specially  affects  the  anterior  tibial  and 
peroneal  groups  in  the  legs,  producing  drop-foot,  and  the  extensors 


PARALYSIS    OF    LOWER    NEURONE    TYPE        233 

ofthe  wrists  and  fingers,  producing  drop-wrist  (Fig.  105).  The 
commonest  causes  of  multiple  neuritis  are  clironic  poisoning  by 
alcohol,  arsenic  (specially  associated  with  cutaneous  eruptions), 
the  diphtheritic  poison,  beri-beri  (associated  with  oedema  of  the 
limbs  and  of  certain  serous  cavities),  diabetes,  septicaemia,  and 
other  poisons.  Lead  neuritis  is  a  peculiar  form  which  practically 
never  attacks  the  sensory  fibres.  The  upper  Hmbs  are  generally 
affected,  the  muscles  attacked  being  the  extensors  of  the  fingers 
and  wrists,  producing  wrist-drop.     The    long    extensors    of    the 


Fig.  105. — Alcoholic  neuritis  with  drop-wrist. 

thumb  become  paralysed  later,  the  extensor  ossis  metacarpi 
poUicis  remaining  unaffected.  The  supinator  longus  usually 
escapes,  so  that  the  disease  contrasts  with  musculo-spiral 
paralysis,  with  which  it  might  be  confused  on  superficial  examina- 
tion. The  blue  line  on  the  gums  and  other  signs  of  plumbism 
also  aid  us  in  the  diagnosis. 

Sometimes  the  lower  motor  neurones  are  paralysed  in  their 
entire  extent,  from  anterior  cornu  to  periphery,  the  disease  com- 
mencing in  the  lowest  spinal  roots  and  spreading  upwards  towards 
the  bulbar  motor  neurones.  This  affection,  known  as  acute  ascend- 
ing "paralysis,  or  Landry's  paralysis,  might  be  confounded  with  an 
ordinary  peripheral  neuritis  were  it  not  for  the  absence  of  sensory 


234  NERVOUS    DISEASES 

changes.  The  paralysis,  commencing  in  the  legs,  and  spreading  up 
the  trmik  to  the  arms,  is  of  the  usual  flaccid  type  with  loss  of 
reflexes.  There  is  no  time  for  muscular  atrophy  or  reactions  of 
degeneration  to  develop,  and  if  the  respiratory  muscles  become 
paralysed  the  patient  dies,  generally  within  a  week  from  the  onset. 
The  sphincters  remain  unaffected.  Various  organisms  have  been 
cultivated  from  the  cerebro-spinal  fluid  and  from  the  peri-dural 
tissues  in  such  cases.  The  spleen  is  frequently  enlarged,  as  in 
certain  other  infective  disorders. 

Before  leaving  the  subject  of  nerve  lesions  of  lower  motor 
neurone  type,  we  must  refer  to  lesions  of  the  cauda  equina, 
the  mass  of  nerve-roots,  lumbar,  sacral  and  coccygeal,  contained 
within  the  lowest  part  of  the  spinal  theca.  According  to  the 
roots  affected,  anterior  or  posterior,  we  have  motor  and  sensory 
symptoms,  both  distributed  in  "  root  "  fashion,  not  according  to 
peripheral  nerves.  The  clinical  picture  varies  according  to  the 
level  of  the  lesion.  When  the  whole  cauda  is  involved,  we  find 
paralysis  (of  lower  motor  neurone  type)  of  all  the  muscles  of  the 
lower  Hmbs,  together  with  anaesthesia  below  the  folds  of  the  groins 
in  front,  including  the  genitals,  and  below  the  upper  part  of  the 
buttocks  behind,  together  with  loss  of  control  of  the  bladder  and 
rectum.  If  the  first,  second,  and  third  lumbar  roots  escape,  the 
anaesthesia  is  less  extensive  (Fig.  20,  p.  35),  sparing  the  upper 
part  of  the  thighs.  If  the  third  lumbar  roots  escape,  thereby 
sparing  the  quadriceps,  the  motor  paralysis  is  correspondingly  less, 
and  the  knee-jerks  survive,  though  there  is  still  paralysis  of  the 
glutei  and  hamstrings  and  of  all  the  muscles  below  the  knees,  with 
loss  of  ankle- jerks  and  paralysis  of  bladder  and  rectum  as  before. 
If  the  lesion  be  lower  still,  the  area  of  paralysis,  motor  and 
sensory,  is  correspondingly  diminished.  Below  the  second  sacral 
roots  there  is  no  paralysis  of  the  lower  Hmbs,  but  there  is  a  char- 
acteristic "  saddle-shaped  "  area  of  anaesthesia  on  the  buttocks, 
perineum,  scrotum  and  penis,  with  a  small  strip  running  from 
the  perineum  down  the  postero-internal  aspect  of  the  thighs. 
Here  also  the  bladder  and  rectum  are  uncontrolled,  and  the  anal 
reflexes  are  lost,  but  there  is    no    motor  weakness  of  the  lower 


PARALYSIS  .  OF    LOWEE    NEURONE    TYPE         235 

limbs,  and  all  the  reflexes  of  the  lower  limbs  are  normal.  And  so 
on,  the  area  of  paralysis  diminishing  as  we  descend,  until  when  there 
is  a  lesion  of  the  fourth  and  fifth  sacral  and  the  coccygeal  roots, 
the  only  signs  are  paralysis  of  the  levator  ani,  with  anaesthesia 
of  the  anus  and  perineum,  the  sphincter  ani  remaining  intact. 

The  chief  difficulty  in  the  diagnosis  of  lesions  in  this  region 
is  to  distinguish  between  a  lesion  of  the  cauda  and  one  of  the 
conus  medullaris — that  part  of  the  spinal  cord  which  extends 
below  the  third  sacral  segment.  In  both  cases  the  motor  power 
of  the  legs  is  unaffected,  and  there  is  anaesthesia  of  the  "  saddle  " 
area,  with  loss  of  sexual  power  and  of  control  of  bladder  and  rectum. 
Cauda  lesions,  however,  are  more  often  gradual  in  onset  than  conus 
affections,  and  are  usually  accompanied  by  intense  sacral  "  root '' 
pains,  and  the  ultimate  anaesthesia  of  a  cauda  affection  is  fre- 
quently preceded  by  cutaneous  hypersesthesia.  A  bed-sore  is 
commoner  in  a  medullary  lesion  than  in  a  cauda  lesion.  Finally 
any  "  dissociation "  of  anaesthesia,  such  as  analgesia  or  therm- 
anaesthesia  without  tactile  anaesthesia,  points  to  a  medullary  lesion. 
If  both  cauda  and  conus  are  included  in  the  same  disease,  the 
cauda  symptoms  mask  the  others. 

Let  us  now  turn  to  motor  palsies  resulting  from  affections  within 
the  muscles  themselves.  Some  of  these  are  really  the  effect  of 
diseases  of  the  intra-muscular  fibrous  tissue.  This  is  the  case  in 
acute  myositis  where  there  is  an  interstitial  inflammation  within 
the  muscle,  often  with  a  good  deal  of  effusion,  so  that  any 
sudden  movement  causes  acute  pain ;  tenderness  on  pressure 
is  also  present.  Lumbago  and  the  famihar  "  stiff  neck "  are 
common  varieties,  and  their  diagnosis  usually  presents  no  diffi- 
culty. TricMniasis  is  a  disease  in  which  the  muscle-fibres  are 
invaded  by  the  trichina  spiralis  worm.  Here  there  is  a  history 
of  the  patient  having  eaten  some  meat,  usually  pork,  which  turns 
out  to  have  been  trichinosed.  Within  a  day  or  two  he  develops 
gastro -intestinal  symptoms  and  becomes  feverish,  with  widespread 
muscular  pains,  rigidity,  and  stiffness,  especially  in  the  muscles 
of  the  limbs.  In  severe  cases  the  pharynx,  tongue,  diaphragm, 
and  even  the  larjmgeal  muscles  may  become  affected.     Together 


236 


NERVOUS    DISEASES 


witli  this,  there  is  a  peculiar  oedema  of  the  face  and  eyelids,  spread- 
ing thence  to  the  limbs,  and  sometimes  to  the  serous  cavities.  The 
blood  contains  a  marked  excess  of  eosinophile  leucocytes,  and  the 
temperature  is  raised.  The  symptoms  last  usually  four  or  five 
weeks. 

Sometimes,  when  a  patient  has  had  his  forearm  fractured  and 
put  up  in  splints,  the  bandages  may  be  applied  too  tightly  and 
the  blood-supply  of  the  muscles  is  interfered  with  by  the  pressure. 
As  a  result  there  are  swelUng  and  pain  in  the  hand,  and  unless 


M^ 

w^^ 

%         .;^ 

^^^i 

Sr- 

:                                                                        'i 

FiG.  lOo, — Ischsemic  myositis. 

the  bandages  be  loosened,  ischgemic  paralysis  (v.  Volkmann)  may 
develop.  This  is  a  variety  of  myositis.  At  first  the  muscles  of 
the  forearm  swell  from  oedematous  effusion ;  later  they  become 
shrunken,  hard,  and  contractured  by  interstitial  fibrous  tissue, 
the  fingers  being  in  a  flexed  position  (see  Fig.  106).  Active  move- 
ments are  lost,  and  even  passive  movements  are  painful.  The 
hardness  and  stiffness  of  the  muscles  and  the  absence  of  R.D., 
together  with  the  normal  condition  of  sensation,  suffice,  with  the 
history  of  the  case,  to  distinguish  it  from  a  neuritis. 

But  we  also  meet  with  cases  of  muscular  weakness  and  atrophy 
localised  in  certain  muscles,  where  the  motor  nerves  and  nuclei 
are  healthy,  but  the  muscle  fibres  themselves  are  primarily  diseased. 
This  group  of  diseases  is  called  muscular  dystrophy,  idiopathic 
muscular  atrophy,  or  myopathy. 


PAKALYSIS    OF    LOWER    NEURONE    TYPE         237 

Clinically  we  recognise  two  main  classes  of  myopathy  : —  (1)  those 
cases  in  which  all  the  affected  muscles  waste  from  the  outset ; 
and  (2)  those  in  which  certain  muscles  undergo  a  false  enlarge- 
ment before  they  ultimately  become  smaller— so-called  pseudo- 
hypertrophic paralysis.  But  there  is  really  no  essential  diiierence 
between  these  two  varieties.  Even  in  pseudo-hypertrophic  cases, 
certain  muscles   undergo   atrophy  from  the   beginning,   whilst  in 


Fig.  107. — Family  of  pseudo-hypertrophic  brothers,  ^t.  4,  8,  and  12. 
The  youngest  and  the  oldest  can  still  stand  and  walk  ;  the  middle 
child  can  no  longer  do  so.  In  the  two  older  boys  the  lower  fibres 
of  the  pectoral  muscles  are  absent. 

the  others  atrophy  and  enlargement  may  be  combined  in  varying 
proportions. 

Muscular  dystrophy  is  a  congenital  disease.  Not  that  the 
symptoms  appear  at  birth,  for  the  child  is  usually  born  apparently 
healthy.  The  age  of  onset  of  noticeable  symptoms  varies  from 
two  to  sixty  years,  though,  most  cases  occur  in  childhood  or  youth. 

The  chief  distinguishing  features  between  myopathic  atrophies 
and  muscular  atrophies  of  nuclear  origin,  spinal  or  bulbar,  are  as 
follows  : — The  age  of  onset  is  earlier,  as  a  rule,  in  myopathy  than 


238 


NERVOUS    DISEASES 


in  progressive  muscular  atrophy  or  amyotrophic  lateral  sclerosis. 
Myopathy  often  runs  in  families  ;  progressive  muscular  atrophy  does 
not.  The  muscles  affected  are  different  in  the  two  cases.  In  pro- 
gressive muscular  atrophy  and  amyotrophic  lateral  sclerosis,  the 
wasting  most  commonly  begins  in  the  small  nmscles  of  the  hands, 
attacking  muscle-groups  corresponding  to  segments  of  the  cord.  In 
myopathy  the  larger  muscles  are  generally  affected,  whilst  the 
small  muscles  of  the  hands  escape.  Amyotrophic  lateral  sclerosis 
tends  to  spread  up  to  the  bulbar  nuclei,  and  to  produce  bulbar 
paralysis.  Myopathy  does  not  cause  bulbar  palsy.  It  is  true 
that  in  one  t}^e  of  myopathy — the  Landouzy-Dejerine — the  face 
is  affected,  and  that  in  pseudo-hypertrophic  cases  the  masseters 
are  sometimes  enlarged;  but  myopathic  palsy  hardly  ever  affects 
the  tongue,  and  never  the  larynx.     In   myopathy  some   of  the 

diseased  muscles  may  be  enlarged, 
whilst  others  are  wasted.  En- 
largement of  muscles  never  occurs 
in  nuclear  disease.  When  a  myo- 
pathic mussle  voluntarily  con- 
tracts, we  may  sometimes  notice 
a  ball  -  shaped  swelhng  in  the 
middle  of  the  muscle,  especially 
in  the  deltoid  or  quadriceps,  which 
is  due  to  the  fact  that  the  dys- 
trophy is  most  marked  at  the 
extremities  of  the  muscles.  The 
long  bones  of  the  limbs  corre- 
sponding to  the  myopathic  muscles 
undergo  a  degree  of  rarefaction 
and  atrophy,  and  the  normal 
ridges  for  muscular  attachments 
become  smoothed  down.^  Fib- 
rillary tremors,  which  are  so  common  in  progressive  muscular 
atrophy,  are  rare  in  myopathy.  Lastly,  in  myopathy,  unhke 
amyotrophic  lateral  sclerosis,'the  deep  reflexes  are  never  increased. 

[  1  Merle  and  Raulot-Lapointe,  N^ouvellelconogi-ajyhie  de  la  Salpetriere,  1909,  No.  3. 


Fig.  108. — Pseudo-hypertrophic  myo- 
pathy. Front  view,  showing  en- 
largement of  calves  and  thighs. 


PARALYSIS    OF    LOWER    NEURONE    TYPE         239 

In  fact,  in  myopathy  the  knee-jerk  may  disappear  from  wasting 
of  the  quadriceps. 


Fig.  101). — Pseudo-hypertrophic  myopathy.     Side  view,  showing 
absence  of  lordosis  in  sitting  posture. 

The  pseudo-hypertrophic  variet}^  of  myopathy  generally  begins 
in  childhood.    It  is  the  most  rapidly  progressive  form  of  myopathy, 


Fig.  110. — Pseudo-hypertrophic  myopathy'.     Showing  method  of 
attaining  the  erect  attitude. 

and  in  most  cases  the  patient  dies  before  attaining  adult  age.  Boys 
are  affected  four  or  five  times  as  often  as  girls.  The  cases  tend  to 
run  in  families,  and  to  select  patients  of  the  same  sex  in  each  family. 
Thus  we  often  find  several  brothers  affected  whilst  the  sisters'escape. 


240  NERVOUS    DISEASES 

But  though,  the  females  generally  escape  themselves,  they  tend  to 
transmit  the  disease  to  their  male  offspring,  so  that  antecedent 
cases  in  a  family  are  always  on  the  mother's  side.  Children  of 
the  same  woman  by  different  husbands  may  suffer  from  the 
disease.  It  is  therefore  unwise  to  marry  a  widow,  however  young 
and  charming,  who  has  a  pseudo-hypertrophic  child.  The  symptoms 
of  pseudo-hypertrophic  paralysis  are  entirely  motor.  The  first 
symptom  which  is  usually  noticed  is  that  the  child  falls  easily,  gets 
up  with  difficulty,  and  cannot  run  or  jump  like  other  children,  nor 


Fig.  111. — Pseudo-hypertrophic  myopathy.     Side  view,  showing 
lordosis  when  standing. 

can  he  walk  on  his  heels,  keeping  the  feet  raised  in  front.  This  weak- 
ness gradually  increases  until  in  a  few  years  the  patient  becomes 
unable  to  stand  or  even  to  sit  up  in  bed.  The  arms  become  weak 
later  than  the  legs.  Figs.  108  to  111  show  two  such  patients.  In 
them  we  notice  the  characteristic  "  pot-belly  "  and  the  lordosis  when 
standing.  The  gait  is  wide -based  and  waddhng,  somewhat  like  that 
of  the  comic-opera  sailor,  and  there  is  often  a  high-stepping  action 
to  clear  the  toes  from  the  ground.  But  most  characteristic  of  all 
is  the  way  in  which  the  patient  rises  from  the  floor  when  placed 


PAKALYSIS    OF    LOWER    NEURONE    TYPE        241 

flat  on  his  back.  He  first  rolls  round  and  gets  on  to  his  hands  and 
knees.  Then,  keeping  his  feet  wide  apart,  he  drags  his  hands  along 
the  floor  towards  his  feet  until  the  knees  are  straightened.  Then 
he  shifts  his  hands  up  to  his  knees  and  proceeds  to  extend  the  hip- 


FlG.  112. — ^Muscular  dystrophy.     Ei'b's  juvenile  type. 

joints  by  chmbing  up  his  thighs.     When  he  has  reached  the  upright 
position,  he  leans  his  trunk  backwards  to  keep  the  hips  extended. 

In  pseudo-hypertrophic  myopathy  certain  muscles  are  specially 
enlarged  and  hard — e.g.  the  calf  muscles  and  the  infra -spinati. 
Other  muscles  may  also  become  enlarged — e.g.  the  quadriceps, 
glutei,  deltoid,  biceps,  and  triceps.     On  the  other  hand,  certain 

Q 


242 


NERVOUS    DISEASES 


otlier  muscles  waste  from  the  first,  without  any  initial  stage  of 
enlargement.  Thus  the  latissimus  dorsi,  teres  major,  and  lower 
fibres  of  the  pectoralis  major  are  often  absent,  so  that  the  folds  of 
the  axilla?  are  poorly  marked,  and  if  we  lift  up  the  child  by  the 
axillae  he  slips  through  our  grasp.     (See  Fig.  107.) 

The  enlarged  muscles  ultimately  shrink  and  become  smaller 
As  the  calf  muscles  shorten,  they  produce  a  talipes  equinus  which 


Fig.  113. — Muscular  dystroph}'.     Erb's  juvenile  type.     Patient 
endeavouring  to  rise  to  standing  posture. 

still  further  hampers  the  walking  powers.  When  the  patient 
becomes  bedridden,  the  contractures  rapidly  attain  an  extreme 
degree.     As  the  quadriceps  wastes,  the  knee-jerk  disappears. 

Primary  atrophic  myopathy  is  a  less  common  type,  and  owing 
to  absence  of  muscular  enlargement,  it  is  more  likely  to  be  confused 
with  progressive  muscular  atrophy  of  spinal  origin.  At  least  three 
varieties  have  been  recognised,  according  to  the  muscles  which  are 
fijst  attacked.  Thus  we  have  (a)  Erb's  juvenile  type,  affecting 
the  muscles  of  the  shoulder-girdles  and  upper  arms ;  (6)  Landouzy 
and  Dejerine's   facio-scapulo-humeral    type,    where    the    atrophy 


PARALYSIS    OF    LOWER    NEURONE    TYPE        243 

begins  in  the  face  ;  (c)  a  type  beginning  in  the  lower  Hmbs,  chiefly 
in  the  anterior  thigh  muscles. 

In  these  atrophic  varieties  there  is  no  striking  preference  for 
boys  ;  both  sexes  are  equally  liable.  The  age  of  onset  too  is 
a  little  later,  commonly  between  15  and  35  years,  except  in  facial 
cases,  where  the  atrophy  may  come  on  in  early  childhood. 

In  ErVs  juvenile  type  the  atrophy  begins  in  the  large  muscles 


Fig.  114. — Muscular  dj-strophy.     Erb's  juvenile  type.     Patient  rising 
to  erect  posture. 

of  the  upper  arms  and  shoulders,  especially  the  biceps,  triceps,  and 
supinator  longus.  Eigs.  112,  113,  and  114  are  from  such  a  patient, 
aged  47,  who  was  a  professional  "  living  skeleton  "  in  a  travelling 
"  freak  "  show.  In  his  case  the  wasting  was  first  noticed  at  the 
age  of  19.  In  some  instances,  as  in  this  particular  case,  the  arms 
and  legs  are  attacked  about  the  same  time.  Or  the  disease  may 
begin  in  the  arms  and  spread  to  the  legs.  The  deltoids  and  spinati 
often  escape,  even  when  the  biceps  and  supinator  longus  are 
wasted,  the  condition  in  this  respect  differing  from  cases  of  spinal 
origin;   and  the  forearm  muscles,  except  the   supinator   longus, 


244 


NERVOUS    DISEASES 


generally    escape    too.       From    weakness     of    the    glutei     and 
quadriceps,    the   patient   when   rising   to   the    standing    posture 


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may  have  to   climb   up  his  legs,  as  does  a  pseudo-hypertrophic 


case. 


The  facio-scapulo-huw.eral  variety  of   Landouzy-Dejerine   com- 


PARALYSIS    OF    LOWER    NEURONE    TYPE 


245 


mences  in  early  life,  the  facial  muscles  being  earliest  affected.  The 
orbiculares  oculorum  and  oris  are  weak,  so  that  the  patient  cannot 
close  his  eyes  tightly  nor  blow  out  his  cheeks  (see  Figs.  115  and 


Fig.  117. — Muscular  dystrophy  ;  type  beginning  in  lower  limbs,  but 
having  advanced  to  upper  limbs.  Patient  pressing  hands  to- 
gether, to  show  atrophy  of  greater  portion  of  pectoral  muscles. 
Intrinsic  muscles  of  hands  unaffected. 


116).  His  lower  hp  droops  and  projects  forwards,  and  his  mouth 
habitually  hangs  open.  The  smile  is  pecuHarly  transverse  and  has 
a  "  forced  "  look,  the  angles  of  the  mouth  being  drawn  outwards 
but  not  upwards.      The  tongue,  ocular  and  jaw  muscles  are  un- 


246 


NEEVOUS    DISEASES 


affected.     Later  the  disease  spreads  to  the  scapular  and  upper-arm 
muscles,  and  finally  to  the  spinal  muscles  and  lower  limbs. 

A  third  type  of  the  disease,  of  which  Figs.  117  and  118  are 
an  example,  begins  in  the  legs,  and  attacks  the  arms  later.  In 
this  patient  the  legs  became  weak  at  the  age  of  12.      When  she 


Fig.  118. 


-Muscular  dystrophy.     Same  patient  as  in  Fig.  117. 
deformity  of  feet. 


Showing 


came  under  observation  at  the  age  of  28  she  was  still  able  to  use 
her  arms,  which  were  contractured  at  the  elbows,  for  knitting  and 
to  feed  herself,  though  she  was  no  longer  capable  of  walking,  owing 
to  claw-foot. 

Other  Varieties  of  Muscular  Wasting. — ^Wasting  of  muscles 
sometimes  occurs  as  a  secondary  phenomenon  in  other  diseases, 
where  there  is  no  implication  of  the  spino-muscular  motor  neurone. 
Thus  the  muscles  may  become  small  from  disuse,  as  may  be  seen 
in  a  limb  which,  owing  to  a  fracture,  has  been  confined  for  several 


PARALYSIS    OF    LOWEE  NEURONE    TYPE        247 

weeks  in  splints.  Disease  of  a  joint  is  generally  accompanied  by 
well-marked  atrophy  of  the  surrounding  muscles.  This  arthritic 
muscular  wasting  specially  affects  the  extensor  muscles  of  the  joint 
— for  example,  the  quadriceps  in  disease  of  the  knee-joint,  the 
interossei  in  osteo-arthritis  of  the  hands,  the  deltoid  in  disease 
of  the  shoulder- joint.  A  degree  of  muscular  wasting  also  occurs 
in  the  paralysed  limbs  in  ordinary  hemiplegia.  Part  of  this  may 
be  the  result  of  disuse,  but  there  are  other  cases  where  the  degree 
of  wasting  is  excessive,  and  disproportionate  to  the  paralysis. 
Lastly,  we  may  meet  with  marked  wasting  of  muscles  in  rare  oases 
of  hysterical  paralysis  (see  Fig.  208,  p.  380).  But  ail  these 
muscular  wastings  can  be  distinguished  from  that  due  to  disease 
of  the  lower  motor  neurone  by  the  absence  of  electrical  reactions 
of  degeneration. 


CHAPTER  XY 

EECURRENT  AND   TRANSIENT   PALSIES 

There  are  certain  forms  of  motor  paralysis  whicli  come  and  go. 
They  tend  to  recur  again  and  again,  and  in  the  intervals  between 
his  attacks  the  patient  is  able  to  execute  all  voluntary  movements 
in  a  normal  or  almost  normal  fashion. 

Of  these  diseases  myasthenia  gravis  is  the  most  serious.  In 
myasthenia  certain  muscles  become  infiltrated  with  deposits  of 
small  round  cells  resembling  lymphocytes,  especially  the  striated 
muscles  innervated  by  the  upper  cranial  nerves,  though  some- 
times the  muscles  of  the  limbs  and  trunk,  and  even  the  respiratory 
muscles,  may  become  affected.  The  disease  is  characterised  by 
the  fact  that  the  patient  becomes,  after  very  moderate  exertion 
of  the  affected  muscles,  abnormally  easily  fatigued,  and  the  affected 
muscles  are,  for  the  time,  paralysed.  The  patient  wakes  up  in 
the  morning  practically  normal,  but  as  the  day  goes  on,  cer- 
tain muscles  gradually  become  paralysed.  Perhaps  the  muscles 
most  often  afEected  are  the  levators  of  the  upper  hds.  Thus 
ptosis  appears,  often  of  unequal  degree  on  the  two  sides  (see  Fig.  119), 
To  this  may  be  superadded  an  external  ophthalmoplegia,  gener- 
ally incomplete.  The  facial  muscles  also  become  weak,  and  the 
patient  has  a  peculiar  "  nasal "  form  of  smile,  in  which  the  angles 
of  the  mouth  are  drawn  upwards  but  very  slightly  outwards.  The 
masseters  and  other  masticatory  muscles  may  also  be  affected,  so 
that  the  patient  cannot  chew  more  than  a  few  mouthfuls.  The 
palate,  tongue  and  larynx  may  all  be  impUcated,  producing  for 
the  time  the  phenomena  of  bulbar  palsy.  In  fact,  the  disease 
was  formerly  named  "  asthenic  bulbar  paralysis."  To  correct  his 
ptosis,  the  patient  may  tilt  his  head  backwards.  But  sometimes 
the  neck  muscles  are  affected,  so  that  the  head  falls  loosely  back 
wards  or  forwards.     In  the  limbs  it  is  chiefly  the  large  proximal 

248 


EECURRENT    AND    TRANSIENT    PALSIES 


249 


muscles  which  are  afiected.  But  the  most  characteristic  feature 
is  the  transitoriness  of  the  paralysis,  and  its  recurrence  on 
slight  exertion.  Thus  the  patient  can  walk  a  short  distance,  but 
soon  has  to  stop  ;  he  may  speak  a  few  sentences,  and  then  his 
voice  becomes  weak  and  his  articulation  indistinct.  In  the 
affected  muscles,  the  electrical  reactions  are  altered  and  we  have 
the    "  myasthenic    reaction."      Faradic    shocks    applied    to    the 


Fig.  119.— Myasthenia  gravis  in  a  man,  of  35.  Marked  weakness  of 
masseters  and  of  lower  facial  muscles  ;  also  right-sided  ptosis. 
The  patient  is  making  a  maximum  effort  to  clench  the  jaws 
and  show  the  teeth. 


muscles  at  first  produce  brisk  contractions,  but  on  repeated  stimu- 
lation the  faradic  excitabiUty  temporarily  disappears.  In  contrast 
to  true  bulbar  palsy,  there  is  no  muscular  atrophy  as  a  rule, 
although  in  very  severe  cases,  slight  wasting  may  supervene.-^ 
The  reflexes,  deep  and  superficial,  together  with  the  sphincters,  are 
unaffected.  If  the  respiratory  muscles  become  severely  affected, 
the  patient  may  die  from  respiratory  failure.  In  addition  to 
1  See  E.  Levi,  Rivista  di  patologia  nervosa  e  mentale,  1906,  p.  450. 


250  NERVOUS    DISEASES 

motor  phenomena  we  may  also  have  evidences  of  fatigue  in  the 
special  senses  and  even  in  common  sensibility.  Thus  the  myas- 
thenic patient  may  have  temporary  impairment  of  visual  acuity 
with  temporary  contraction  of  the  visual  fields,  and  in  rare  cases 
temporary  diminution  of  sensation  has  been  observed  in  the 
limbs.^ 

Thomson's  disoaso  or  "myotonia  congenita,"  is  a  rare  congenital 
affection  of  the  voluntary  muscles,  which  appears  to  be  due  to 
their  possessing  an  excessive  proportion  of  undifferentiated  sarco- 
plasm  and  muscle-nuclei,  and  relatively  too  small  a  proportion  of 
the  anisotropic  or  fibrillar  element.  This  latter  contracts  briskly, 
whereas  sarcoplasm  contracts  very  slowly.  In  Thomsen's  disease, 
whenever  the  patient  starts  to  perform  a  voluntary  movement, 
his  muscles  are  thrown  into  a  state  of  tonic  spasm,  which 
does  not  relax  at  once  but  passes  off  gradually,  the  muscles 
slowly  becoming  supple,  until  at  length  he  can  perform  the 
movement,  say  that  of  walking,  in  a  normal  fashion  ("  ce 
n'est  que  le  premier  pas  qui  coute  ").  But  if  he  stops  and  starts 
again,  or  if  he  tries  to  hurry  his  original  speed,  this  stiffness 
reappears,  and  has  again  to  be,  as  it  were,  worked  off.  The 
lower  Hmbs  are  most  commonly  affected,  the  affected  muscles 
often  being  somewhat  enlarged,  but  other  muscles  may  also  show 
the  phenomena.  Thus  the  patient's  eyes  may  remain  temporarily 
firmly  closed  after  a  cough  or  sneeze,  his  mouth  may  remain 
open  after  a  yawn,  and  so  on.  The  sensory  functions  and  the 
reflexes  are  unaffected.  But  the  affected  muscles  have  a  char- 
acteristic reaction  to  electrical  stimulation.  Their  excitabihty 
is  increased  to  both  faradism  and  galvanism.  To  galvanism 
KCC  is  equal  to  AGO  (instead  of  being  greater,  as  in  health), 
and  the  contraction  set  up,  whether  by  galvanism  or  by  fara- 
dism, is  remarkably  persistent,  lasting  for  a  time  after  the  stimulus 
has  ceased.     The  disease  runs  in  families. 

Eulenberg's  disease  or  "paramyotonia  congenita,"  is  a  family 
affection  somewhat  like  Thomsen's  disease,  in  which  a  tonic  spasm 
appears  in  certain  voluntary  muscles,  more  particularly  in  the  face, 

^  Tilney  and  Mitchell  Smith,  Neurocjraphs,  1911,  vol.  i.  p.  178. 


RECURRENT    AND    TRANSIENT    PALSIES  251 

so  that  the  patient  is  unable,  for  a  quarter  of  an  hour  or  longer, 
to  open  his  eyes  or  to  speak.  Less  often  the  muscles  of  the 
limbs  are  affected.  The  condition,  however,  differs  from  Thomsen's 
disease  in  its  immediate  exciting  cause.  The  tonic  spasm  of 
Eulenberg's  disease  is  excited  not  by  exertion  but  by  cold,  and 
is  generally  reheved  by  warmth.  The  two  diseases,  however,  are 
closely  allied,  and  have  been  observed  coincidently  in  members  of 
the  same  family.^ 

Myotonia  atrophica  "^  is  a  rare  disease,  intermediate  in  its 
characters  between  the  myotonias  and  the  myopathies.  It  some- 
times occurs  in  several  members  of  the  same  family.  The  patients 
are  more  often  males  than  females,  and  the  symptoms  usually 
appear  in  adult  hfe.  The  myotonic  phenomena  generally  precede 
the  muscular  wasting.  The  first  symptom  is  usually  a  difficulty 
in  relaxing  the  grasp.  Myotonic  phenomena  in  other  muscles  are 
sHghter  in  degree,  and  are  chiefly  seen  in  the  muscles  of  mastica- 
tion, the  facial  muscles  and  the  tongue  ;  they  are  rare  in  the 
lower  limbs.  Atrophy  of  myopathic  type  appears  later,  irregular 
in  its  distribution,  chiefly  afiecting  the  facial  muscles,  the  sterno- 
mastoids  and  the  vasti  muscles  of  the  thighs.  It  may  also  be 
present  elsewhere  in  lesser  degree,  as  in  the  forearm  muscles  and 
the  dorsiflexors  of  the  foot. 

Another  interesting  variety  of  transient  paralysis  is  known 
as  intermittent  limp  or  "dysbasia  angio-sclerotica "  ("clau- 
dication intermittent  s "  of  Charcot,  or  the  "  intermittiiendes 
Hinken  "  of  German  authors).  An  analogous  condition  in  horses, 
known  as  "  spring-halt,"  has  been  familiar  to  veterinary  surgeons 
for  many  years.  The  patient  is  most  commonly  a  man  of  middle 
age,  sometimes  of  gouty  constitution,  who  very  often  has  been  an 
inveterate  tobacco-smoker.  The  symptoms  are  very  character- 
istic. At  rest  he  feels  no  disability.  But  when  he  begins  to  walk, 
though  he  starts  off  normally,  he  soon  begins  to  feel  his  legs  tired, 
heavy  and  painful.  A  cramp-hke  pain  appears  and  gradually 
becomes  intolerable,  making  him  limp ;  and  if  he  perseveres  with 

1  Delprat,  Deutsche  med.  W ochenschrift,  1892,  s.  158. 

^  Rossolimo,  Nouvelle  Iconographie  de  la  Salpetriere,  1902,  p.  63.  Batten  and 
Gibb,  Brain,  1909,  p.  187. 


252  NERVOUS    DISEASES 

his  attempt,  lie  finally  becomes,  for  the  time,  totally  unable  to 
walk  a  single  step.  He  rests,  the  pain  and  weakness  pass  off, 
only  to  return  when  he  starts  to  walk  afresh.  If  we  examine  such 
a  patient  during  a  paroxysm  of  temporary  incapacity,  we  find 
his  feet  and  legs  cold,  and  perhaps  purple  or  mottled  red.  But 
what  is  most  characteristic  of  all  is  that  the  pulse  in  the  feet,  in 
the  posterior  tibial  or  the  dorsalis  pedis  artery,  is  absent  or  nearly  so. 
There  are  no  sensory  changes,  the  reflexes  are  normal,  and,  except 
during  the  paroxysms,  the  motor  power  of  the  limbs  is  unimpaired. 
All  these  phenomena  appear  to  be  the  result  of  a  temporary  spasm 
of  the  arteries  of  the  limb  (the  arteries  themselves  being  frequently 
already  narrowed  by  arterio-sclerosis),  so  that  during  walking 
an  increased  blood-supply  to  the  muscles  is  not  forthcoming, 
hence  there  result  temporary  anaemia,  pain  and  weakness  in  the 
affected  muscles.  In  rare  instances  similar  phenomena  have  been 
observed  in  the  arms. 

Rare  cases  have  also  been  observed  where  a  hemiplegia, 
partial  or  complete,  sometimes  accompanied  by  aphasia,  occurs 
in  an  elderly  patient,  indistinguishable  at  first  from  an  ordinary 
cerebral  hsemorrhage  or  thrombosis.  But  within  a  few  hours 
all  the  hemiplegic  phenomena  suddenly  disappear,  leaving  the 
patient  perfectly  normal.  The  patient  may  have  a  series  of  such 
attacks  of  transient  hemiplegia  at  intervals  of  days,  weeks  or 
months.  For  over  three  years  I  watched  the  case  of  an  elderly 
cabman  who  had  numerous  attacks  of  left  hemiplegia  lasting  for 
a  day  or  so,  leaving  him  absolutely  well  in  the  intervals.  Another 
case  of  mine  was  in  a  vigorous  business  man,  aged  jQfty-one,  who 
had  frequent  attacks  of  temporary  aphasia  with  right  hemiplegia. 
Similar  cases  have  also  been  recorded  by  Grasset  ^  and  by  Lang- 
will.^  Such  cases  may  be  termed  angiospastic  hemiplegia,  and  are 
probably  due  to  temporary  spasm  of  one  middle  cerebral  artery, 
analogous  to  the  spasm  of  peripheral  vessels  in  intermittent  limp. 
They  must  be  carefully  distinguished  from  the  transient  hemi- 
plegia which  is  not  uncommon  in  general  paralysis  of  the  insane. 

1  Revue  neurologique,  May  30,  1906. 
^  Scottish  Medical  and  Surgical  Journal,  Jixne  1906. 


REOUREENT    AND    TRANSIENT    PALSIES  253 

Amongst  the  transient  paralyses  we  must  also  bear  in  mind  the 
various  craft-palsies,  professional  cramps,  or  occupation  neuroses,  in 
which  the  limb  is  normal  for  all  motor  actions  except  one  particular 
movement — often,  unfortunately,  the  one  on  which  the  patient's 
livehhood  depends.  The  commonest  variety  is  the  so-called  writer's 
cramp  or  scrivener's  palsy,  though  we  also  meet  with  similar  con- 
ditions in  the  cramp  of  pianists,  vioHnists,  telegraphists,  typists, 
tailor's  cutters,  hair-cutters,  hammer-men,  cow-milkers,  watch- 
makers, harpists,  cigarette-makers,  sempstresses,  and  so  on.  The 
cramp  comes  on,  not  during  the  period  when  the  sufferer  is  learning 
his  occupation,  but  after  he  has  become  an  expert  and  requires 
to  perform  the  particular  skilled  movement  repeatedly  for  prolonged 
periods.  For  all  other  movements  except  that  particular  one,  the 
hmb  is  normal.  Thus  in  writer's  cramp  the  patient  can  use 
his  hand  normally  for  piano-playing  or  for  grasping  and  using  a 
heavy  tool.  This  is  because  the  weakness  is  not  due  to  muscular 
but  to  cerebral  fatigue.  A  professional  cramp  does  not  appear  in 
its  fully  developed  form  at  first,  but  passes  through  different  stages 
of  severity.  In  the  shghtest  variety  there  is  simply  a  degree  of 
stiffness  or  spasm  in  performing  the  act,  with  a  subjective  sensation 
of  pain  and  of  intense  mental  discomfort  and  fatigue.  In  other  cases 
a  temporary  paralysis  appears  when  the  patient  attempts  to  write, 
so  that  the  pen  can  no  longer  be  held  in  the  hand.  In  still  more 
severe  cases  tremor  is  superadded  to  spasm  in  the  affected  muscles. 
The  diagnosis  is  easy,  inasmuch  as  the  phenomena,  whether  spastic 
or  paralytic  or  perhaps  a  combination  of  both,  only  supervene  when 
the  one  skilled  motor  action  is  performed,  and  the  same  muscles 
can  be  used  for  all  other  actions  without  pain,  spasm  or  weakness. 

There  is  also  a  curious  hereditary  disease  known  as  "family 
periodic  paralysis."  This  malady  may  run  through  several  suc- 
cessive generations  of  the  same  family,  attacking  one  or  more 
members  of  the  same  generation.  Males  and  females  are  both 
liable.  The  patient,  who  is  otherwise  apparently  healthy,  has 
attacks  of  flaccid  paralysis  of  all  four  limbs,  recurring  irregularly 
without  apparent  exciting  cause.  The  duration  of  a  paroxysm 
varies  from  two  or  three  days  down  to  a  few  hours.     The  attacks 


254  NERVOUS    DISEASES 

generally  come  on  during  the  night  when  the  patient  is  in  bed. 
He  wakes  up  and  finds  himself  more  or  less  widely  paralysed. 
First  the  legs  are  affected,  later  the  arms,  and  last  of  all  the 
muscles  of  the  trunk  and  neck.  The  cranial  nerves  usually  escape. 
In  the  Hmbs  the  paralysis  stai-ts  proximally  and  the  distal  parts 
are  affected  last,  so  that  the  patient  may  still  be  able  to  move 
his  toes  and  fingers  when  he  has  lost  all  power  in  the  hips  and 
shoulders.  In  severe  cases  the  intercostal  muscles  may  also  be 
paralysed.  Most  striking  of  all  is  the  fact  that  during  these 
paroxysms  of  flaccid  palsy  the  affected  muscles,  for  the  time,  lose 
their  excitabOity  to  faradic,  galvanic,  or  mechanical  stimulation, 
and  all  the  reflexes  in  the  affected  Arabs  disappear.  Sensation  is 
unimpaired  and  the  sphincters  are  unaffected.  An  additional  point 
is  that  during  the  paroxysm,  the  left  ventricle  becomes  temporarily 
dilated,  as  can  be  proved  by  percussion  and  occasionally  by  the 
appearance  of  a  systolic  mitral  bruit.  The  muscular  paralysis 
passes  off  in  the  reverse  order  to  that  in  which  it  came  on.  The 
toes  and  flngers  recover  before  the  proximal  muscles,  and  the 
muscles  earhest  attacked  are  the  last  to  recover.  The  patient 
then  remains  apparently  normal  until  his  next  attack,  weeks  or 
months  later. 

Sudden  attacks  of  hemiplegia  may  also  occur  in  general 
paralysis  of  the  insane,  constituting  a  variety  of  so-called  "  con- 
gestive attacks."  But  although  the  patient  may  recover  rapidly 
from  his  hemiplegia,  often  within  a  few  days,  he  is  not  a  normal 
individual,  for  careful  physical  examination  will  always  reveal 
evidences  of  the  disease,  mental  or  physical,  e.g.  facial  tremors, 
pupillary  changes,  or,  most  constant  of  all,  lymphocytosis  of  the 
cerebro -spinal  fluid. 

Amongst  other  transient  affections  we  may  mention  those 
of  muscular  cramp  and  of  tetany.  The  conditions  are  easily 
recognised,  and  may  temporarily  interfere  with  the  movements 
of  the  affected  Umbs.  Both  are  painful  affections,  tetany  being 
most  commonly  seen  in  infants,  whilst  cramp  is  most  often  met 
with  in  healthy  adolescents  or  adults  who  have  been  performing 
some   unwonted    prolonged    muscular   effort.       Cramp   is   also   a 


EECUERENT    AND    TRANSIENT    PALSIES         255 

distressing  symptom  in  cholera,  in  some  cases  of  diabetes,  and 
occasionally  in  exophthalmic  goitre.  Tetany  is  generally  bilateral, 
and  has  a  characteristic  posture  of  the  hands  and  feet  (see  Fig. 
33,  p.  76). 

Occasionally  we  see  patients  who  complain  that  their  legs 
suddenly  give  way  in  the  street,  causing  them  to  fall.  This  may 
be  due  to  various  causes.  For  example,  it  is  a  not  uncommon 
symptom  in  tabes.  The  tabetic  patient  often  has  hypotonia  of 
the  muscles  about  the  knees  and  also  deficient  joint-sense,  a  com- 
bination of  phenomena  which  may  make  him  fall  unexpectedly. 
In  such  a  case  the  condition  of  the  deep  reflexes,  the  state  of  the 
pupils,  and  the  other  phenomena  of  tabes  render  the  diagnosis 
easy.  Other  cases  of  sudden  falling  are  due  to  minor  epilepsy, 
where  the  patient  has  an  attack  of  momentary  unconsciousness 
during  which  he  falls,  but  recovers  consciousness  at  once  and  gets 
up  again,  not  knowing  why  he  has  fallen.  Here  the  diagnosis 
will  depend  on  the  observation  of  other  epileptiform  attacks,  major 
or  minor.  We  should  particularly  inquire  for  the  occurrence  of 
sudden  pallor  of  the  face  or  fixity  of  expression,  indicating  a  passing 
attack  of  petit  mal,  too  slight,  perhaps,  to  produce  a  fall. 

In  other  cases,  again,  we  have  to  do  with  sudden  vertigo, 
as  in  Meniere's  disease,  causing  the  patient  to  fall.  Such  cases 
are  recognised  by  the  concomitant  auditory  phenomena  (see  p.  161) , 
and  by  the  fact  that  they  are  not  associated  with  loss  of 
consciousness. 

Sudden  weakness  of  a  hmb  may  occur  iu  hysteria,  especially 
after  some  emotional  shock.  Hysterical  paralysis  may  persist 
for  variable  periods  of  time,  varying  from  a  few  hours  to 
many  weeks  or  months.  The  paralysis  not  uncomm.only 
recovers  as  suddenly  as  it  came  on,  sometimes  under  emotional 
or  rehgious  excitement,  under  hypnotic  suggestion,  or  under 
energetic  stimulation,  electric  or  thermal,  for  example,  that  of 
a  Pacquehn  cautery.  Hysterical  paralysis  never  attacks  a  single 
muscle,  but  always  a  group  of  muscles.  It  is  never  accom- 
panied by  reactions  of  degeneration,  no  matter  how  much  the 
hysterical    limb    may   be   wasted.     We   diagnose  hysteria   by    a 


256  NEEVOUS    DISEASES 

process  of  exclusion,  noting  not  only  tke  absence  of  certain  signs 
of  organic  disease,  but  looking  also  for  the  presence  of  various 
hysterical  "  stigmata,"  to  which  we  shall  refer  later. 

But  we  must  not  forget  that  in  many  cases  of  apparently 
hysterical  and  transient  paralysis  in  young  women,  the  patient 
after  one  or  more  of  such  attacks  may  afterwards  develop  the 
signs  of  disseminated  sclerosis.  The  onset  of  disseminated  sclerosis 
may  be  indistinguishable  from  an  attack  of  hysterical  paralysis, 
the  weakness  of  the  limb  in  both  diseases  may  be  transient  and 
may  apparently  clear  up  completely  for  a  time.  But  a  series  of 
such  attacks  should  always  raise  in  our  minds  the  suspicion  of  an 
underlying  disseminated  sclerosis  and  should  make  us  give  a  guarded 
prognosis,  especially  if  the  patient  has  had  more  than  one  attack 
of  weakness,  not  necessarily  in  the  same  limb.  We  should  pay 
particular  attention  to  the  state  of  the  optic  discs.  Early  optic 
atrophy  will  exclude  mere  hysteria,  so  also  will  an  extensor 
plantar  reflex  or  anything  approaching  a  true  nystagmus.  In 
fact,  the  disease  which  is  most  often  wrongly  diagnosed  as  hysteria 
is  incipient  disseminated  sclerosis. 


CHAPTER    XVI 

INCO-ORDINATION 

A  NEWLY-BORN  child  Cannot  co-ordinate  the  movements  of  its 
limbs.  Certain  co-ordinated  vital  actions,  such  as  sucking,  swallow- 
ing, respiration,  &c.,  are  performed  well  from  birth,  but  in  an 
infant's  hmbs  the  movements  are  mostly  of  an  aimless  restless 
character,  with  the  exception,  perhaps,  of  grasping  movements  of 
the  hands.  And  even  these  latter  differ  from  the  co-ordinated 
grasp  of  later  life,  inasmuch  as  the  infant's  thumb  is  hardly  used 
at  all  for  opposition,  and  the  flexion  movement  of  the  fingers 
occurs  chiefly  when  some  object  comes  in  contact  with  the  hand, 
the  movement  being  reflex  rather  than  voluntary. 

The  child  only  learns  after  long  practice  to  use  its  muscles  in 
such  a  fashion  as  to  produce  properly  co-ordinated  movements  of 
the  Umbs.  Walking,  writing,  swimming,  the  playing  of  any  game, 
are  all  performed  awkwardly  at  first.  Skill  is  at  last  attained 
by  frequent  repetition,  and  once  a  co-ordinated  action  has  been 
thoroughly  learned,  the  effort  for  its  performance  becomes  in- 
finitesimal, so  that  in  time  it  is  performed  more  or  less  auto- 
matically. 

Every  co-ordinated  action  involves  contraction  not  only  of  the 
so-called  prime-movers  but  of  their  antagonists,  and  if  these  two 
groups  are  not  properly  balanced,  the  attempted  movement  is 
awkward  and  jerky.  This  condition  occurs  in  a  number  of  diseases 
and  is  termed  ataxia  or  inco-ordination.  This  means  clumsiness, 
unsteadiness,  or  awkwardness  in  the  performance  of  movements  in 
a  non-paralysed  patient  who  was  previously  able  to  execute  these 
movements  in  normal  fashion. 

In  testing  for  ataxia  of  the  upper  limbs,  we  ask  the  patient 
to  perform  such  an  action  as  picking  up  a  small  object,  say 
a    pin,  from    a    smooth    surface.     If    he    is    ataxic,  he    fumbles 

257  -D 


258  NERVOUS    DISEASES 

during  the  attempt,  or  may  perhaps  pounce  on  the  object  in  a 
sudden,  jerky  fashion.  Another  useful  test  is  to  ask  the  patient 
to  hft  a  brimming  glass  of  water  to  his  lips  and  notice  whether 
he  spills  it.  Or  we  may  ask  him  to  touch  rapidly  the  tip  of  his 
nose  with  each  index  finger  in  succession.  If  he  is  ataxic,  his 
finger  misses  his  nose  by  a  greater  or  smaller  interval,  or,  on 
reaching  it,  the  finger  shows  additional  oscillatory  movements. 
Other  good  tests  for  ataxia  are  to  make  the  patient  button  or 
unbutton  his  coat  or  collar,  or  to  write  with  a  fine-pointed  pen. 
In  every  case,  we  should  observe  whether  the  unsteadiness  is 
increased  or  unchanged  when  the  patient  shuts  his  eyes.  Slight 
degrees  of  ataxia  due  to  sensory  impairment  may  be  noticed 
only  when  the  patient  is  deprived  of  the  help  of  his  visual 
impressions. 

In  the  case  of  the  lower  limbs  we  detect  moderately  severe 
ataxia  by  observing  the  patient's  gait,  asking  him  to  walk 
"  heel-and-toe  "  along  a  straight  line,  then  to  turn  sharply  and 
come  back.  In  well-marked  locomotor  ataxia  the  gait  is  broad- 
based,  the  feet  are  lifted  too  high  and  the  heels  are  brought  down 
with  a  stamp.  In  ceretellar  disease,  on  the  other  hand,  the 
patient  reels  or  lurches  along,  being  especially  unsteady  when 
turning  round  (see  later,  "  Postures  and  Gaits ").  To  detect 
ataxia  of  a  single  lower  limb,  we  ask  the  patient  to  place  one  heel 
on  the  opposite  knee,  or  to  trace  with  one  foot  a  circle  or  some 
other  pattern  on  the  floor,  or  we  ask  him  when  lying  down  to 
touch  with  his  toe  our  own  finger  held  in  the  air.  And  here  also, 
in  ataxia  of  the  lower  limbs,  we  should  always  note  whether  the 
patient's  unsteadiness  is  increased  or  unchanged  by  shutting  the 
eyes.  In  tabetic  ataxia  of  the  lower  limbs,  the  unsteadiness  is 
increased  when  the  eyes  are  shut.  Romherg^s  sign  consists  in  the 
tendency  of  a  patient,  who  can  stand  steadily  with  the  eyes  open, 
to  fall  when  he  closes  them.  Thus  an  early  sign  of  tabes  is  the 
so-called  "  wash-basin "  sign,  where  the  patient  falls  into  his 
basin  when  washing  his  face.  A  minor  degree  of  Romberg's  sign 
can  often  be  detected  in  the  earlier  stages  of  tabes,  where  the 
patient  is  still  able  to  stand  with  the  eyes  shut,  but  the  tendons 


INCOORDINATION  259 

on  the  dorsum  of  the  foot  are  seen  to  exhibit  irregular  restless 
contractions,  the  so-called  "  danse  des  tendons." 

Ataxia  of  the  bulbar  muscles  has  already  been  referred  to  (see 
Dysarthria,  p.  109).  As  to  ataxia  of  the  muscles  of  the  trunk, 
its  diagnostic  significance  is  less  than  that  of  the  limbs,  inasmuch 
as  by  the  time  that  the  trunk  muscles  are  recognisably  ataxic,  the 
limbs  already  show  very  marked  unsteadiness.  Ataxia  of  the 
head  and  trunk  muscles  is  evidenced  by  swaying  movements  when 
the  patient  sits  up. 

Having  detected  ataxia  in  the  movements  of  any  limb,  we  must 
always  determine  the  condition  of  the  sensory  impulses  from  that 
limb,  testing  not  only  the  various  forms  of  cutaneous  sensibility 
but  also  the  deep  sensations,  especially  the  kinsesthetic  sense  and, 
still  more  important,  the  joint-sense.  Finally,  we  must  determine 
the  condition  of  the  deep  reflexes,  noting  their  exaggeration  as  in 
disseminated  sclerosis,  or  their  abolition  as  in  tabes  or  in  Friedreich's 
ataxia.     We  also  note  the  type  of  plantar  reflexes. 

The  commonest  variety  of  ataxia  is  that  due  to  deficiency  of 
peripheral  impressions — not  so  much  from  the  skin  as  from  the 
deeper  structures,  the  muscles  and  joints.  Thus  in  lesions  of  feri- 
fheral  sensory  nerves  an  ansesthetic  limb  is  often  ataxic.  Division 
of  the  fosterior  roots  of  the  brachial  plexus,  the  anterior  roots  re- 
maining intact,  causes  marked  ataxia  of  the  upper  limb.  In  fact 
such  a  patient  may  be  totally  unable  to  move  the  limb  if  his  eyes 
are  closed,  so  that  he  no  longer  has  the  guiding  influence  of  vision. 
Degeneration  of  the  posterior  roots  and  posterior  columns,  as 
in  tahes,  produces  marked  ataxia.  A  tabetic  patient  is  ataxic 
because  of  deficiency  of  afferent  impressions,  more  especially  from 
his  muscles  and  from  his  joints.  If  the  muscle-tonus  is  lost  and 
the  muscles  are  hypotonic,  as  in  many  cases  of  tabes,  the  patient 
has,  as  it  were,  to  "  pull  in  the  slack  "  before  the  muscles  come 
into  proper  play,  thereby  making  the  movement  jerky,  inharmonious, 
and  flail-like.  Joint-sense  being  impaired,  he  has  to  perform 
a  maximal  movement  in  order  to  get  the  sensation  of  having 
moved  the  joint  at  all.  Thus  in  walking  when  he  lifts  his  leg, 
owing  to  want  of  proper  joint-sense,  he  throws  the  limb  up  with 


260  NERVOUS    DISEASES 

abnormal  suddenness  and  to  an  unnecessary  height  in  order  to 
gain  the  sensation  of  flexion  of  the  joint.  He  then  stamps 
it  down  with  excessive  emphasis  to  make  sure  that  it  really 
is  extended.  Such  a  patient  with  ataxia  of  sensory  origin  com- 
pensates for  the  deficiency  of  sensory  impressions  from  his  hmbs 
by  means  of  his  vision.  When  watching  his  partially  ansesthetic 
limbs,  he  can  control  them  better.  Hence  if  he  closes  his  eyes, 
the  regulating  influence  of  vision  is  lost  and  he  becomes  much 
more  ataxic.  This  is  the  probable  explanation  of  Romberg's 
sign  in  tabes. 

Ataxia  similar  to  that  of  tabes  also  occurs  in  other  organic 
cord  lesions  implicating  the  posterior  columns,  as,  for  instance,  in 
tumours  or  chronic  sclerosis  of  the  posterior  columns,  whether  com- 
bined or  not  with  lateral  sclerosis — e.g.  some  cases  of  disseminated 
sclerosis  or  spinal  syphilis.  In  such  diseases  the  other  signs  and 
symptoms  guide  us  to  a  correct  diagnosis. 

Ataxia  combined  with  spasticity  occurs  in  the  early  stage  of 
subacute  combined  degeneration  of  the  spinal  cord,  generally  a 
disease  of  middle  life.  This  disease  occurs  chiefly  in  conditions  of 
profound  anaemia.  In  the  first  stage  of  the  malady  there  are  loss 
of  joint-sense  and  subjective  sensations  of  tingling,  &c.,  in  the 
lower  limbs,  not  unlike  tabes,  but  with  increased  knee-jerks  and 
extensor  plantar  reflexes.  Vibration-sense  in  the  bones  of  the 
lower  limbs  is  lost  long  before  any  cutaneous  anaesthesia 
develops.  After  lasting  for  weeks  or  months  the  disease 
then  changes  its  type,  and  in  this  second  stage  the  spastic 
paraplegia  becomes  severe  and  marked  anaesthesia  develops  in 
the  lower  limbs  and  trunk.  Lastly,  and  usually  abruptly,  within 
a  few  days  the  type  changes  once  more,  and  there  is  a  terminal 
stage  of  flaccid  paraplegia  lasting  a  few  weeks,  with  absolute 
anaesthesia  of  the  lower  limbs  and  trunk,  loss  of  the  knee-jerks, 
the  plantar  reflexes  remaining  extensor  in  type.  The  paralysed 
muscles  rapidly  waste  and  lose  their  faradic  excitabiHty.  The 
bladder  and  rectum  are  uncontrolled  and  the  lower  limbs  become 
cedematous.  The  whole  disease  from  start  to  finish  lasts  about 
two  or  three  years. 


INCO-ORDINATION 


261 


But  a  patient  may  be  ataxic  when  all  his  peripheral  sensations 
are  normal.  This  occurs  in  the  different  varieties  of  cerebellar 
ataxia.  Let  us  take,  for  example, 
Friedreich'' s  ataxia,  a  develop- 
mental disease  affecting  mainly 
the  afferent  tracts  in  the  cord 
leading  upwards  to  the  cerebel- 
lum, which  is  the  centre  for 
automatic  co  -  ordination  (the 
cerebellum  itself  being  intact). 
In  Friedreich's  ataxia  the  patient 
becomes  ataxic,  as  in  tabes,  but 
with  the  cutaneous  and  joint- 
sense  intact.  The  ataxia  is 
unaffected  by  closing  the  eyes. 
The  age  of  the  patient,  who  is 
commonly  an  adolescent,  the 
presence  of  scoliosis,  of  manus 
cava,  and  of  pes  cavus  (Figs. 
120  and  121),  the  normal  pupil- 
lary reactions,  the  presence  of 
nystagmus,  the  absence  of  light- 
ning pains  or  of  bladder  trouble, 
all  serve  to  distinguish  this  dis- 
ease from  tabes,  though  in  both 
diseases  the  deep  reflexes  are 
absent.  The  plantar  reflexes  in 
tabes  are  flexor  in  type,  whilst 
in  Friedreich's  ataxia  they  are  of 
the  extensor  variety. 

Well-marked  ataxia  com- 
bined with  muscular  atrophy,  absence  of  deep  reflexes,  and 
deformity  of  the  feet  and  hands,  also  occur  in  family  hyper- 
trophic interstitial  neuritis.  In  this  disease,  however,  unhke 
Friedreich's  ataxia,  we  never  have  an  extensor  plantar  reflex, 
whilst  there  are  well-marked  sensory  changes  in  the  limbs. 


Fig.  120.- 


-Friedreich's  ataxia, 
scoliosis. 


Showino; 


262 


NERVOUS    DISEASES 


Ataxia  also  occurs  in  certain  localised  lesions  of  the  medulla 
oblongata.  Thus,  for  example,  a  unilateral  lesion  may  interrupt 
the  fibres  of  the  direct  cerebellar  tract  and  thereby  interfere  with 
co-ordination  of  the  ipso-lateral  limbs.  Such  a  lesion  (com- 
monly the   result    of    thrombosis  of  the  posterior  inferior  cere- 


FiG.  121. — Friedreich's  ataxia.     Showing  pes  cavus  and  manus  cava. 

bellar  artery),  which  usually  interrupts  at  the  same  time  the  fibres 
of  Gowers'  tract,  may  extend  inwards  to  imphcate  the  inter-olivary 
arcuate  fibres  and  the  fillet,  together  with  the  nuclei  of  the  lower 
cranial  nerves.  It  produces  a  characteristic  unilateral  bulbar 
syndrome.^     The  symptoms  are  as  follows  : — From  interruption  of 

1  Babinski  and  Nageotte,  Revue  neurologique,  1902,  p.  358. 


INCO-ORDINATION  263 

the  cerebellar  afferent  fibres  there  is  ataxia  (or  asynergia)  of  the 
ipso-lateral  limbs.  From  interference  with  the  tract  for  paiji  and 
temperature  we  have  analgesia  and  therm-ansesthesia  of  the 
opposite  side  of  the  body  (see  Fig.  11,  p.  17).  From  inter- 
ference with  the  oculo-pupillary  centre  in  the  bulb  there  is 
myosis  and  pseudo-ptosis  (see  later,  "  Cervical  Sympathetic 
Paralysis,"  p.  336),  and  there  may  be  difficulty  of  deglutition  due 
to  affection  of  the  cranial  nerve  nuclei.  If  the  lesion  extends 
forwards  to  implicate  the  pyramid  of  the  same  side,  there  is 
hemiplegia  of  the  contra-lateral  arm  and  leg. 

Mane's  hereditary  cerebellar  ataxia,  due  to  primary  parenchy- 
matous degeneration  of  the  cerebellum  itself,  is  somewhat  similar 
to  Friedreich's  ataxia,  but  there  is  no  loss  of  knee-jerks,  and  the 
age  of  onset  is  somewhat  later.  Olivo-ponto-cerebellar  atrophy  is 
a  disease  described  originally  by  Dejerine  and  Thomas,  in  which 
there  is  a  primary  atrophy  of  the  cerebellar  cortex,  the  bulbar 
olives,  the  grey  matter  of  the  pons,  the  middle  cerebellar 
peduncles,  and  sometimes  the  restiform  bodies.  Clinically  there 
is  marked  ataxia  or  asynergia.  The  disease  does  not  run  in 
families,  and  its  onset  is  in  advanced  life. 

Cerebellar  ataxia  also  occurs  in  cerebellar  tumoms,  in  vascular 
lesions  of  the  cerebellum,  in  disseminated  sclerosis  affecting  the 
cerebellum  or  its  peduncles,  in  cerebellar  abscess,  in  encephahtis 
of  the  cerebellar  cortex,  an  acute  disease  of  febrile  onset  which  is 
sometimes  met  with  in  children,  and  it  occurs  occasionally  in  old 
age  as  the  result  of  a  primary  senile  atrophy  of  the  cerebellar 
cortex,  especially  affecting  the  Purkinje  cells. ^ 

Cerebellar  ataxia,  better  termed  cerebellar  asynergia,  differs 
ill  several  important  respects  from  the  ataxia  due  to  deficient 
afferent  impressions.  It  is  chiefly  evidenced  in  the  cerebellar 
gait,  which  has  a  staggering,  reefing  character,  fike  that  of 
a  drunken  man,  but  without  the  stamping  of  the  true  tabetic. 
We  recognise  several  factors  in  the  production  of  cerebellar 
ataxia.  Part  of  the  ataxia,  |- especially  that  of  the  trunk 
muscles,  is  due  to  vertigo,  the  patient  being  unsteady  in  his  gait 

^  Rossi,  Nouvelle  Iconographie  de  la  Salpetriere,  No.  1,  1907. 


264  NERVOUS    DISEASES 

because  he  feels  giddy.  A  cerebellar  gait  therefore  occurs  in  many- 
cases  of  labyrinthine  disease.  If  a  cerebellar  patient  Ues  down, 
his  vertigo  is  diminished  and  there  being  no  longer  any  effort  re- 
quired to  maintain  equihbrium,  his  movements  are  much  less  un- 
steady. Another  factor  in  cerebellar  ataxia  is  the  existence  of 
the  muscular  hypotonia  which  we  often  meet  with  in  cerebellar 
disease  ;  this  hypotonia,  in  unilateral  cerebellar  lesions,  is  more 
marked  in  the  limbs  of  the  affected  side.  The  third  and  most 
important  factor  in  cerebellar  ataxia  is  the  want  of  the  co-ordinat- 
ing influence  of  the  cerebellum  on  the  cerebral  m.otor  cortex.  This 
connection  is  a  crossed  one,  the  right  cerebellum  being  connected 
with  the  left  cerebral  cortex,  vid  the  right  superior  cerebellar 
peduncle  and  the  left  red  nucleus.  Some  tumours  of  the 
frontal  lobe  are  associated  with  cerebellar  ataxia,  probably  owing 
to  indirect  interference  with  the  functions  of  the  contra-lateral  side 
of  the  cerebellum.  True  cerebellar  ataxia,  unlike  the  ataxia  of 
tabes  dorsalis,  is  uninfluenced  by  closure  of  the  eyes. 

Ataxia  also  occurs  in  some  affections  of  the  higher  cerebral 
centres.  For  example,  there  are  certain  toxic  affections  in  which 
the  patient  becomes  ataxic.  The  most  f  amiUar  variety  is 
that  of  acute  alcoholic  intoxication.  Part  of  this  ataxia  may 
possibly  be  due  to  cerebellar  intoxication,  but  a  large  part  of  it 
is  cerebral,  as  evidenced  by  the  "  mental  ataxia,"  the  disordered 
articulation,  &c.  The  temporary  ataxia  of  fatigue,  of  writer's 
cramp  and  of  other  occupation-neuroses  is  also  probably  of  cerebral 
origin,  so  also  is  the  transient  ataxia  which  sometimes  follows 
enteric  fever  or  other  exanthemata. 

There  are  certain  diseases  of  the  cerebral  cortex,  in  which  ataxia 
is  distinct.  In  chorea  the  patient  not  only  exhibits  spontaneous 
involuntary  movements,  but  he  also  has  distinct  ataxia  on  volun- 
tary movement.  In  organic  monoplegia  or  hemiplegia,  especially 
when  shght  in  degree  and  amounting  merely  to  paresis,  distinct 
ataxia  often  exists  in  the  paretic  limbs.  Hemi-ataxia  is  one  of 
the  characteristic  phenomena  in  lesions  of  the  optic  thalamus.  In 
such  cases  the  limbs  on  the  side  contra -lateral  to  the  lesion  are 
not    only    ataxic    but    also    partially    anaesthetic    with    loss    of 


INCO-ORDINATION  265 

joint-sense,  whilst  spontaneous  pains  in  the  affected  Hmbs  are 
commonly  present.  Sometimes  ataxia  of  the  Hmbs  precedes  an 
attack  of  hemiplegia — pre-hemiplegic  ataxia,  especially  in  threatened 
softening  from  arterial  thrombosis.  More  often  the  ataxia  appears 
dm:ing  convalescence  from  a  slight  hemiplegic  attack  —  fost- 
hemiplegic  ataxia,  where  the  patient  has  to  learn  the  process  of 
co-ordination  again  in  his  paretic  Hmbs.  This  form  of  ataxia  must 
be  distinguished  from  athetosis,  the  involuntary  slow  writhing 
movements  of  the  limbs  which  occurs  in  old  and  severe  cases  of 
hemiplegia,  especially  of  infantile  hemiplegia. 

Ataxia  is  one  of  the  most  striking  signs  of  disseminated 
sclerosis,  where  the  unsteadiness  of  the  limbs  is  often  associated 
with  a  superadded  coarse  oscillatory  tremor — the  so-called  inten- 
tion-tremor. How  much  of  the  unsteadiness  in  disseminated 
sclerosis  is  due  to  cerebral  and  how  much  to  cerebellar  disease 
it  is  difficult  to  say  in  any  individual  case.  Intention  tremor 
is  also  present  in  some  cases  of  family  hypertrophic  interstitial 
neuritis  (see  above,  p.  227).  The  tremor  of  hemiplegic  distribution 
which  is  observed  in  the  Hmbs  in  cases  of  lesions  of  the  red 
nucleus  or  rubro-spinal  tract  (see  p.  86)  is  present  at  rest,  but 
becomes  exaggerated  on  voluntary  movements,  rendering  them 
ataxic.  In  this  respect  it  contrasts  with  the  tremor  of  paralysis 
agitans,  which  can  usually  be  controlled  to  permit  of  the  per- 
formance of  a  voluntary  movement. 

Finally  we  may  meet  with  ataxia  of  the  most  varied  types 
in  hysteria.  Here  the  affection  is  probably  one  which  impli- 
cates the  highest  psychical  centres.  The  diagnosis  of  hysterical 
ataxia  rests  on  the  presence  of  other  stigmata  of  hysteria,  to- 
gether with  the  absence  of  evidence  of  organic  disease.  Some- 
times hysterical  ataxia  is  associated  with  "  cortical "  anaesthesia 
of  the  affected  limb.  In  such  a  case  the  patient  may  be  able 
to  move  the  limb  normally  with  her  eyes  open,  but  when  they 
are  closed  ataxia  appears.  This  does  not  necessarily  occur  in 
every  hysterically  anaesthetic  Hmb,  for  in  many  cases  profound 
anaesthesia  may  be  present  without  ataxia.  The  diagnosis  of 
hysterical  ataxia,  however,  seldom  presents  much  difficulty  to  a 


266  NERVOUS    DISEASES 

careful  observer.  The  disease  wHch.  is  most  often  mistaken  for 
hysteria  is  disseminated  sclerosis  in  its  earher  stages.  In  both 
diseases  we  may  have  a  history  of  transient  weakness  of  a  limb, 
apparently  clearing  up  completely  for  a  time.  But  in  disseminated 
sclerosis  there  are  objective  evidences  of  organic  disease  in  the 
form  of  pallor  of  the  optic  discs,  nystagmus,  alterations  of  the 
abdominal  and  plantar  reflexes,  sphincter  trouble,  and  so  on. 


CHAPTER  XYII 

POSTURES    AND    GAITS 

Postures. — In  health  the  posture  of  the  body  and  of  its  various 
members  is  determined  partly  by  gravity,  partly  by  the  relative 
strength  of  the  muscles  at  the  various  joints.  Therefore, 
inasmuch  as  the  flexor  muscles  of  our  limbs  are  usually  more 
powerful  than  the  extensors,  the  ordinary  posture  of  the  limbs 
at  rest  is  one  of  slight  flexion.  This  is  easily  verified  by 
observing  a  sleeping  child.  In  the  erect  attitude  the  muscles 
of  special  importance  in  maintaining  equilibrium  are  the  ex- 
tensors of  the  hips  and  knees  ;  whilst  in  standing  on  one  foot 
the  peronei  are  of  particular  importance  by  inclining  the  whole 
lower  limb  outwards  from  the  ankle  up,  and  bringing  the  centre  of 
gravity  over  the  foot.  The  minor  varieties  of  posture  in  different 
healthy  individuals,  which  we  learn  to  recognise  as  part  of  each 
man's  personal  characteristics,  are  largely  the  result  of  differ- 
ences not  only  in  muscularity  but  of  habit.  The  pose  of  a 
powerful,  muscular  man  is  widely  different  from  that  of  a  thin, 
debihtated  invahd.  Moreover,  if  fi'om  exercise  or  want  of  exercise, 
certain  groups  of  muscles  are  more  or  less  developed  than  the 
normal,  the  posture  is  further  modified,  even  in  health.  For 
example,  we  all  know  the  characteristic  straddHng  gait  of  the 
professional  jockey. 

Similar  principles  apply  to  those  cases  of  organic  disease  where 
certain  muscles  or  groups  of  muscles  are  affected  by  paralysis. 
Paralysed  Umbs  gradually  assume  characteristic  postures,  and  these 
postures  of  organic  disease  are  not  matters  of  haphazard,  but  are 
determined  by  anatomical  rules. 

If  the  muscular  paralysis  be  the  result  of  a  lower  motor 
neurone  lesion,  in  the  anterior  cornua,  anterior  nerve-roots,  nerve 
trunks    or  muscle-fibres,  the  paralysed  muscles  become  wasted. 

267 


268 


NERVOUS    DISEASES 


Their  unopposed  non-paralysed  antagonists  slowly  become  con- 
tracted, and   fix   the   Hmb  in   a   certain  definite  posture   which 
is  best  demonstrated  if  the  patient  tries  to  throw  the  paralysed 
muscles  into  action,  in  which  case  the  antagonists  contract  alone. 
For  example,  Fig.  122  is  a  photograph  of  a  woman  who  had 


Fig.  122.— Chronic  myelitis  of  fifth  cervical  segment,  with  atrophic 
paralysis  of  deltoid,  biceps  and  supinators. 

a  localised  lesion  in  the  anterior  cornua  of  the  cord  at  the  level 
of  the  fifth  cervical  segment.  Amongst  the  chief  muscles  supplied 
by  the  anterior  cornua  at  that  level  are  the  deltoid,  biceps  and 
supinators.  These  muscles  underwent  atrophy  and  their  unopposed 
antagonists  became  contracted.  As  a  result  we  see  that  from 
paralysis  of  the  deltoid  and  contraction  of  its  opponents  the  shoulder 


POSTURES    AND    GAITS  269 

is  adducted,  similarly  from  paralysis  of  the  biceps  the  elbow  is 
extended  by  its  opponents,  and  from  paralysis  of  the  supinators 
the  forearm  is  hyperpronated  by  their  antagonists.  This  posture  is 
characteristic  of  a  cord  lesion  at  the  fifth  cervical  segment. 

Fig.  123  shows  the  posture  assumed  in  a  case  of  paralysis  of  the 
external  popliteal  nerve.       This  nerve  was  divided   by  a   bullet- 


FiG.  123. — Paralysis  of  external  popliteal  nerve  of  right  leg,  the  result 
of  a  bullet-wound.     Showing  muscular  atrophy  and  drop-foot. 

wound  in  an  officer's  right  leg.  In  addition  to  anaesthesia  corre- 
sponding to  the  cutaneous  distribution  of  the  nerve,  the  figure 
shows  the  presence  of  foot-drop  due  to  paralysis  of  the  anterior  tibial 
group  of  muscles,  with  unopposed  contraction  of  the  calf  muscles. 
Here,  of  course,  the  action  of  gravity  is  a  factor  as  well,  the  weight 
of  the  foot  tending  to  increase  the  foot-drop. 

Fig.  124  shows  the  posture  in  a  case  of  paralysis  of  the 
musculo-spiral  nerve.  The  patient  is  trying  to  extend  both  his 
wrists.     On   the   paralysed   side   we   notice   the   atrophy   of   the 


270  NERVOUS    DISEASES 

supinator  longus  and  the  paralysis  of  the  extensors  of  the  wrist 
and  fingers,  also  the  characteristic  swelling  on  the  dorsum  of  the 
hand,  probably  bursal  in  origin,  which  appears  in  long-standing 
cases  of  drop-wrist. 

Lower  motor  neurone  lesions  affecting  the  muscles  of  the  hand 
produce  certain  highly  characteristic  postures  : — 

(1)   The   so-called   monkey-hand    [main    de   singe),    in   which 


Fig.  124. — Case  of  claw-baud  from  rupture  of  first  thoracic  root,  fol- 
lowing a  dislocation  of  the  right  shoulder.  Note  the  atrophy  of 
intrinsic  muscles  of  the  right  hand  ;  also  the  pseudo-ptosis  on 
that  side,  due  to  affection  of  cervical  sympathetic. 

there  is  a  localised  wasting  of  the  thenar  muscles  with  loss  of  the 
power  of  opposing  the  thumb. 

(2)  Claw-hand,  or  inain  en  griffe,  due  to  paralysis  of  the  inter- 
ossei  and  lumbricales,  in  which  the  fingers  are  now  controlled  by 
the  long  flexors  and  extensors  alone.  In  this  condition  the 
proximal  phalanges  become  hyper-extended,  whilst  the  two  distal 
phalanges  are  flexed  in  a  hook-like  fashion.  Meanwhile  the  power 
of  abducting  the  fingers  by  the  interossei  is  lost.  When  the  ulnar 
nerve  alone  is  paralysed  the  deformity  is  more  marked  in  the  two 


POSTUEES    AND    GAITS 


271 


ulnar  fingers,  since  the  lumbricales  corresponding   to  the  index 
and  middle  fingers  (supplied  by  the  median  nerve)  escape. 

(3)  The  preacher's  hand  (main  de  prMicateur),  specially 
common  in  syringomyelia.  In  this  variety,  from  survival  of  the 
long  extensors,  the  hand  is  extended  or  even  hyper-extended,  at 
the  wrist.  The  loss  of  the  movements  of  adduction  and  abduc- 
tion in  the  extended  fingers,  due  to  interosseal  paralysis,  develops 
when  the  "  main  de  singe  "  becomes  the  "  main  en  griff e."  As  a 
matter  of  fact,  these  three  positions  of  the  hand  occur  in  lesions 


Fig.  125. — Loft-sided  musculo-spiral  paralysis.     Showing  drop-wrist 
and  atrophy  of  supinator  longus. 

not  only  of  the  anterior  cornua  (as  in  progressive  muscular 
atrophy,  syringomyeha,  amyotrophic  lateral  sclerosis),  but  also  in 
anterior -radicular  lesions,  in  lesions  of  the  lower  roots  of  the 
brachial  plexus  (see  Fig.  124),  in  toxic  or  infective  neuritis,  in 
leprosy,  in  family  neuritic  diseases  like  peroneal  muscular  atrophy 
and  hypertrophic  interstitial  neuritis. 

If  the  paralysis  be  due  to  an  upper  motor  neurone  lesion, 
the  law  which  determines  the  posture  is  different.  We  no 
longer  have  atrophic  paralysis,  Hmited  to  a  particular  muscle  or 
muscles  as  in  a  lower  motor  neurone  lesion.  Instead,  there 
gradually  develops  a  spastic  paralysis,  in  which  all  the  muscles 


272  NEKVOUS    DISEASES 

of  the  affected  limb  or  segment  of  a  limb  are  more  or  less  paralysed 
and  in  a  state  of  hyper-tonus.  The  muscles  which  are  normally 
more  powerful  are  therefore  placed  at  an  advantage  during  the 
process  of  spastic  contracture,  and  a  posture  results  which  is  an 
exaggeration  of  the  normal  attitude  at  rest,  so  that,  for  example,  in 


Fig.  vKx  Fig.  127. 

Case  of  left-sided  infantile  hemiplegia  in  a  patient  aged  7  years.  Onset 
of  hemiplegia  five  years  previously.  Showing  posture  of  limbs.  In 
Fig.  126  note  athetosis  of  left  fingers.  In  Fig.  127  note  inversion 
of  ankle  and  dravfing  up  of  heel. 

a  chronic  hemiplegia  the  familiar  posture  of  the  upper  hmb  is  that 
of  flexion  with  pronation,  that  of  the  lower  hmb  being  one  of 
slight  flexion  at  the  hip  and  knee,  with  extension  and  inversion 
of  the  ankle,  and  a  tendency  to  dorsiflexion  of  the  toes  (see  Figs. 
126  and  127). 

This  spastic  posture  in  hemiplegia  does  not  come  on  at  once. 


POSTURES    AND    GAITS 


273 


There  is  an  initial  flaccid  stage,  lasting  several  weeks  or  even 
months,  before  the  spastic  rigidity  sets  in.  (In  a  small  number 
of  cases  the  hemiplegia  may  remain  permanently  flaccid.)  But 
even  during  this  flaccid  stage  the  postures  of  the  hemiplegic  limbs 


Fig.  128. 


Fig.  129. 


From  a  case  of  right-sided  hysterical  hemiplegia  in  a  left-handed  patient. 
Showing  contractures  of  hand  and  foot.  The  right  forearm  was 
rigidly  sapinated,  but  is  being  passively  semi-pronated  by  the 
physician,  to  show  the  posture  of  the  hand. 

are  often  different  from  those  of  the  unaffected  side  at  rest.     One 
of  the  most  characteristic  signs  is  an  apparent  broadening  of  the 


Fig.  130. — Functional  paraplegia.     Showing  longitudinal  fold  of  soles. 

lower  limb  (Heilbronner's  ^  "  breites  Bein  ").  This  consists  in  an 
outward  rotation  of  the  lower  hmb  at  the  hip-joint,  due  to  its 
own  weight  when    in  the  recumbent   posture    (analogous  to  the 


1  Deutsche  Zeitschrift  fiir  Nervenheilkunde,  Bd.  28,  1904,  s.  1. 

S 


274 


NEKVOUS   DISEASES 


displacement  which,  occurs  in  fracture  of  the  neck  of  the  femur). 
The  thigh,  therefore,  when  looked  at  from  the  front,  appears  broader 
than  on  the  healthy  side.  Moreover,  the  flaccid  paralysed  muscles 
fall  back  by  their  own  weight,  and  on  transverse  section  the  thigh 
forms  a  flattened  oval  instead  of  an  approximate  circle  as  on  the 


FiGr.  131. — Left-sided  hysterical  hemiplegia  with  glosso-labial  spasm 
on  protrusion  of  tongue.  The  left  upper  limb  was  also  rigidly  con- 
tracted at  the  shoulder  and  elbow,  the  hand  being  flaccid. 


healthy  side.  This  apparent  broadening  of  the  paralysed  thigh  can 
be  well  seen  if  the  patient  be  seated  on  a  hard,  flat  seat.  It  does 
not  occur  in  hysterical  hemiplegia. 

In  functional  paralysis  the  conditions  are  different.  Hysteria, 
it  is  often  said,  may  simulate  organic  disease — thus  we  may  have 
functional    hemiplegia,    paraplegia,    or   monoplegia.      But   if   we 


POSTUEES    AND    GAITS 


275 


$ 


examine  carefully  we  usually  find  that  this  similarity  is  more  or 
less  rough  and  inaccurate.  And  why  ?  Because  hysterical  con- 
tractures are  not  governed  by  anatomical  rules  ensuring  the  pre- 
ponderance of  the  stronger  muscles.  Hysterical  contractures 
usually  present  some  points  in  which  they  difEer  from  the  postures 
of  genuine  organic  lesions.  Thus,  for  ex- 
ample, we  do  not  have  loss  of  deep 
reflexes  nor  muscular  atrophy  with  R.D. 
as  in  lower  motor  neurone  lesions  ;  nor 
do  we  have  an  extensor  plantar  reflex 
nor  a  true  clonus  as  in  genuine  pyra- 
midal disease.  Moreover,  if  hysterical 
hemiplegia  affects  the  face  we  have,  not  a 
true  paralysis,  but  a  glosso-labial  hemi- 
spasm. Figs.  128  and  129  are  from  a  case 
of  functional  hemiplegia,  in  which  the 
contracture  alone  was  enough  to  distin- 
guish it  from  an  organic  case.  Instead  of 
the  usual  flexed  and  pronated  postme  of 
the  upper  limb,  we  observe  that  the  elbow 
and  wrist  are  extended,  the  forearm  is 
supinated,  and  the  fingers  are  half-bent 
in  a  hook-hke  fashion,  whilst  in  the 
lower  Hmb  the  inversion  of  the  ankle  is 
overdone,  out  of  all  proportion  to  the 
ordinary  equinus  position.  The  con- 
tracture in  this  patient  appeared  sud- 
denly, as  is  so  often  the  case  in  hysteria, 
unlike  the  gradual  development  of  an  organic  contracture.  Fig. 
130  shows  a  peculiar  contracture  of  the  soles  in  another  case  of 
hysterical  paraplegia,  in  which  the  feet  had  a  fold  running  longi- 
tudinally along  the  soles,  totally  unlike  any  organic  contracture. 

Fig.  131  shows  a  case  of  left-sided  hysterical  hemiplegia,  in 
which  the  contracture  of  the  upper  Hmb  differs  from  that  of 
organic  disease  ;  for  whilst  the  shoulder,  elbow  and  wrist  are  rigid, 
the  fingers  are  flaccid — a  combination  which  does  not  occur  in 


Fig. 132 


Hyper-extension  of 
knees  in  a  case  of  tabes — 
"genu  recurvatum." 


276 


NEEVOUS   DISEASES 


organic  hemiplegia.  We  also  observe  tliat  this  patient  has  glosso- 
labial  hemispasm.  When  she  protrudes  her  tongue  it  deviates 
considerably  to  the  paralysed  side,  but  in  such  an  exaggerated 
fashion  that  it  is  easy  to  recognise  the  deformity  as  spasmodic, 
not  paralytic.  We  also  note  that,  when  the  tongue  is  protruded, 
the  face  on  the  paralysed  side  goes  into  a  state  of  spasm,  so  that 
the  left  naso-labial  fold  is  deeper  than  on  the  healthy  side,  a 
condition  which  is  the  reverse  of  what  we  find  in  organic  hemi- 


FiG.  133. — Tabetic  hypotonia  of  popliteal  muscles. 

plegia.  Glosso-lahial  hemispasm  such  as  this  is  not  a  common 
sign,  but  when  it  occurs  it  is  pathognomonic  of  hysteria. 

Hysterical  contractures  often,  but  not  always,  disappear  during 
sleep  or  during  deep  ansesthesia.  If  the  contracture  has  persisted 
for  months,  adhesions  may  form  in  the  joints,  so  that  even  under 
an  ansesthetic  the  contracture  may  not  completely  relax,  and  we 
may  have  to  break  down  the  adhesions  forcibly. 

The  postures  of  organic  paralyses,  then,  whether  supra-  or 
infra-nuclear,  are  definite  and  comparatively  simple,  being  governed 
by  the  anatomical  rules  we  have  mentioned.  Hysterical  postures, 
on  the  other  hand,  being  under  no  such  restrictions,   may  assume 


POSTURES    AND    GAITS  277 

the  most  varied  and  weird  appearances,  examples  of  which  might 
be  multiplied  indefinitely.      Whether   spastic   or    paralytic,    the 


Fig.  134. — Tabetic  hypotonia  of  gluteal  and  hamstring  muscles. 

motor  phenomena  of  hysteria  are  usually  "  systematised."  As 
Babinski  has  pointed  out,  they  merely  affect  one  or  more 
"  systems  "  of  voluntary  movements  which  the  muscles  of  the 


Fig.  135. — Tabetic  hypotonia  of  muscles  of  lower  limbs  and  trunk. 

face  or  of  a  limb  are  called  on  to  perform.  Hysterical  postures 
are  caricatures  or  exaggerations  of  some  spastic  or  paralytic 
posture,  which,  however,  never  corresponds  in  distribution  to  a 
peripheral  nerve  nor  to  a  spinal  segment  but  to  some  well- 
recognised    attitude.        Therefore    a    hysterical     paralysis    or    a 


278  NEEVOUS    DISEASES 

hysterical  contracture  can  always  be  imitated,  whereas  an 
organic  contracture  is  never  accurately  imitated  by  a  hysterical 
patient. 

In  many  cases  of  tabes  dorsalis  there  is  marked  deficiency  of 
muscular  tonus,  a  condition  known  as  hypotonia.  This  slackness  of 
the  muscles  has  a  remarkable  influence  on  the  patient's  postures. 
Thus,  for  example,  hypotonia  of  the  peronei  increases  the  difficulty 
of  standing,  since  whenever  the  patient  lifts  one  leg,  the  other 
fixed  leg  is  no  longer  pulled  outwards  as  in  health  to  bring  the 


Fig.  138. — Tabetic  hypotonia  of  adductor  muscles. 

centre  of  gravity  over  the  fixed  foot.  When  the  hamstrings  and 
sural  muscles  behind  the  knee  are  hypotonic  (see  Fig.  132),  the 
joint  becomes  hyper-extended  in  the  erect  posture — the  so-caUed 
"  genu  recurvatum  " — unlike  the  knee-joint  of  a  healthy  individual, 
in  which,  however  strongly  the  knee  be  extended,  there  always  re- 
mains a  concavity  behind.  This  hypotonia  of  the  pophteal  muscles 
produces  another  very  characteristic  sign  of  tabes,  which  is 
that  when  the  patient  hes  in  bed  with  the  knee  extended,  the 
heel  can  be  passively  raised  whilst  the  back  of  the  knee  re- 
mains in  contact  with  the  bed  (see  Fig.  133).  Hypotonia  of 
the  muscles  of  the  trunk  and  lower  limbs  in  tabes  may  permit 
of  the  patient  assuming  the  most  extraordinary  postures  without 
pain — postures  which  are  impossible  to  any  ordinary  individual 


POSTUKES    AND    GAITS  279 

who  is  not  a  professionally  trained  contortionist  (see  Figs.   134, 
135  and  136). 

Amyotonia  congenita  (sometimes,  though,  less  aptly,  called 
iiiyatonia  congenita)  is  a  condition  of  extreme  flaccidity  of  the 
muscles,  which  are  soft  and  lax  on  palpation.  When  thrown  into 
voluntary  contraction  they  do  not  harden  like  ordinary  muscles, 
and  it  may  be  impossible  by  palpation  to  distinguish  them  from 
the  subcutaneous  tissues.  The  joints  are  flail-like,  and  can  be 
placed  in  all  sorts  of  fantastic  postures  (see  Fig.  137).     There  is  no 


Fig.  137. — Amyotonia  congenita  in  a  child  of  2^  years, 
showing  inability  to  sit  up. 

true  motor  paralysis,  although  voluntary  movements  are  devoid 
of  vigour.  The  amyotonia  is  most  marked  in  the  lower  limbs. 
The  sphincters  are  unaffected.  The  electric  excitability  is 
diminished  both  to  faradism  and  to  galvanism,  but  without 
polar  changes.  The  child  can  bear  strong  faradic  stimulation 
with  unusual  stoicism.  The  deep  reflexes  are  absent,  whilst  the 
cutaneous  and  organic  reflexes  are  normal.  The  condition 
is  a  congenital  one,  closely  allied  to  myopathy,  with  which  it 
is  sometimes  combined.  The  phenomena  are  usually  detected 
within  the  first  twelve  months  after  birth.  Sometimes  the 
symptoms  improve,  and  the  deep  reflexes  may  even  return,  but 
the  patient  never  attains  normal  muscular  power.  Pathologically 
the  muscles  show  changes  identical  with  those  found  in 
primary  myopathy. 


280  NERVOUS    DISEASES 

Gaits. — Unlike  some  of  the  lower  animals — for  example,  the 
chicken  or  the  lamb — the  human  infant  at  birth  cannot  stand  or 
walk.  It  is  not  until  the  child  reaches  the  age  of  about  eighteen 
months  that  he  begins  to  walk.  First  he  learns  to  stand,  and  then 
after  repeated  efforts  he  succeeds  in  walking.  During  the  process 
of  learning,  he  reels  and  falls  about  just  like  an  adult  with  cerebellar 
disease. 

We  do  not  all  of  us  walk  exactly  in  the  same  fashion.  Even 
healthy  individuals  show  minor  differences  in  gait.  An  old  man 
walks  differently  from  a  youth,  a  soldier  differently  from  a 
sailor,  and  a  woman  advanced  in  pregnancy  differently  from  a 
maiden.  The  wearing  of  ordinary  boots  with  artificial  heels 
also  modifies  ths  gait,  so  that  in  health  the  first  part  of  the 
boot  to  show  signs  of  wear  is  usually  the  back  of  the  heel  on  the 
outer  side.  Ladies'  high-heeled  boots  modify  the  gait  still  more, 
throwing  the  weight  of  the  body  unduly  forwards  towards  the 
heads  of  the  metatarsal  bones. 

When  testing  the  gait  in  cases  of  nervous  disease  it  is  advisable 
to  have  the  patient's  lower  limbs  well  exposed,  and  without  boots. 
To  get  a  good  view  of  the  limbs  it  is  well  to  have  a  minimum 
of  clothing  on  the  patient.  A  good  plan  is  to  have  him 
clad  in  some  light  garment  like  a  shirt,  whose  tail  is  pulled  for- 
wards between  the  legs  from  behind  and  pinned  in  front,  thereby 
leaving  the  upper  limbs  free.  We  ask  the  patient  to  walk  straight 
away  from  us  towards  some  given  point,  then  to  turn  round  and 
come  back. 

In  a  normal  gait  the  limbs  are  moved  forward  easily,  the  feet 
neither  scraping  the  ground  whilst  being  lifted,  nor  being  unduly 
stamped  down  as  they  descend.  The  forward-moving  or  "  active  " 
leg  is  the  one  which  carries  the  weight  of  the  body.  The  trunk  and 
pelvis  therefore  lean  a  httle  towards  the  corresponding  side  during 
the  "  active  "  phase  of  each  limb.  This  trunk  movement  is  attained 
partly  by  the  action  of  the  gluteal  muscles,  partly  by  the  sacro- 
lumbar  muscles  of  the  same  side.  A  short,  thick-set  person  with 
a  broad  pelvis  tends  to  have  a  "  waddhng  "  gait,  as  the  weight 
of    his    trunk    is    shifted    across    from    one    side    to    the    other. 


POSTURES    AND    GAITS  281 

When  the  gluteal  muscles  are  weak,  the  patient  waddles 
excessively,  in  his  ejffiorts  to  throw  his  weight  to  each  side 
alternately. 

The  gait  is  altered  in  various  diseases.     Thus  it  may  become 
spastic,  ataxic,  reehng,  high-stepping,  and  so  on. 


Fig.  138. — Spastic  diplegia.     Showing  "  scissor-gait." 

A  spastic  gait  occurs  in  lesions  of  the  pyramidal  tract — for 
example,  in  hemiplegia,  in  diplegia,  and  in  spastic  paraplegia.  In 
organic  hemi'plegia  the  active  forward- projection  of  the  hmb  is 
especially  difficult  on  the  paralysed  side,  and  the  weight  of  the  body 
has  to  be  carried  forwards  by  the  aid  of  the  other  side  plus 
gravity,  unUke  the  normal  gait  where  the  weight  is  carried  entirely 
by  the  "  active  "  advancing  leg.  Thus  when  the  hemiplegic  leg 
ought  to  be  in  the  "  active  "  phase,  it  is  not  properly  flexed  at 


282  NERVOUS   DISEASES 

the  knee  or  ankle,  nor  is  it  actively  pushed  forwards  but  merely 
dangles  forward  hke  a  pendulum,  not  directly  forwards,  but  swing- 
ing in  a  circular  fashion  round  the  opposite  hip  as  on  a  pivot. 
When  the  "  active  "  phase  of  the  non-paralysed  limb  occurs,  the 
hemiplegic  foot  (owing  to  weakness  of  the  peronei  and  dorsiflexors 
of  the  ankle,  with  over-action  of  the  inverters  and  calf  muscles) 
stays  on  the  ground  too  long,  thereby  scraping  the  front  part  of 
the  foot,  especially  the  ball  of  the  great  toe ;  the  stride  of  the 
paralysed  limb  is  therefore  shorter  than  on  the  healthy  side.  In  a 
case  of  spastic  diplegia,  or  double  hemiplegia,  the  patient  is  unable 
to  project  either  leg  forwards  in  the  ordinary  way,  but  has  to  jerk 
each  forwards  in  turn  with  a  circular  swing,  so  that,  in  a  well- 
marked  case,  not  only  does  the  patient  take  abnormally  short  steps, 
catching  the  ball  of  each  foot  on  the  ground,  but  from  the  circular 
swing  of  the  limbs,  together  with  their  adductor  spasm,  they  cross 
alternately  in  front  of  each  other,  producing  the  cross-legged  or 
"scissor  "  gait  (see  Fig.  138).  Meanwhile  the  trunk  and  upper  limbs 
make  violent  jerky  movements,  swinging  the  body  from  one  side  to 
the  other.  In  ordinary  spastic  paraplegia  from  cord  disease,  there 
is  not  the  cross-legged  gait  of  diplegia,  but  the  patient  moves 
stiffly  along,  taking  abnormally  short  steps,  the  front  part  of  the 
feet  clinging  to  the  ground,  thus  wearing  out  the  toes  of  the  boots. 
Meanwhile  the  tendency  to  ankle-clonus  causes  a  "  trepidation  "  of 
the  whole  body  in  severe  cases,  from  tremor  of  the  feet.  Such 
a  patient  stumbles  over  the  slightest  obstacles. 

The  gaits  of  hysteria  are  of  the  most  varied  types.  For  example, 
in  hysterical  hemiplegia,  the  patient  often  pushes  the  paralysed 
foot  along  the  ground  as  if  on  a  skate,  or  drags  it  helplessly  along 
with  its  dorsum  resting  on  the  ground,  as  seen  in  Fig.  139. 
If  this  is  bilateral,  the  patient  is  totally  unable  to  walk  or 
stand.  Or  the  foot  may  be  held  in  a  position  of  tahj)es 
calcaneus,  or  the  patient  may  walk  on  the  outer  border  of  the 
foot  (see  Fig.  140)  when  walking,  even  when  no  such  posture  is 
present  at  rest ;  or  one  lower  limb  may  be  acutely  flexed  at  the 
hip  and  knee,  so  that  the  patient  has  to  use  crutches. 

Or    again,  the  patient  may  have  a  zig-zag  gait,  or  he  may 


POSTURES    AND    GAITS 


283 


throw  one  leg  about  with  a  wild  flourish  before  bringing  it  to  the 
ground,  or  may  suddenly  kneel  down  every  few  steps — these  are 
tics  of  gait.  Astasia- ahasia  is  the  term  applied  to  a  condition  in 
which  a  hysterical  patient  is  unable  to  stand  or  walk,  although 
capable  in  the  recumbent  posture  of  performing  all  movements  of 
the  lower  limbs  normally.  The  varieties  of  hysterical  gaits  are 
practically  unhmited,  but  every  one  of  them  differs  in  some 
respect  from  the  gait  of  organic  disease. 


Fig.  139.— Gait  in  a  case  of  left-sided  hysterical  hemiplegia.     The  marks 
on  the  left  leg  are  scars  of  self-inflicted  burns. 


The  side-gait  (Schiiller's  "  Flankengang  ")  is  a  useful  means  of 
diagnosing  between  organic  and  hysterical  hemiplegia.  To  test  it, 
the  patient  is  placed  on  a  line  and  made  to  move  along  it  side- 
ways in  a  given  definite  direction — say,  towards  the  right.  A 
normal  individual  during  this  movement,  first  leans  his  trunk  to 
the  left,  then  balancing  his  weight  on  the  left  leg,  he  hfts  the 
right  from  the  ground,  abducts  it  by  a  muscular  effort,  brings  the 
trunk  erect  again,  puts  down  the  right  foot,  last  of  all  hfting  the 
left  leg,  adducting  it  and  placing  it  alongside  the  right.     How  is 


284 


NERVOUS    DISEASES 


this  performed  in  organic  hemiplegia  ?  We  find  that  the  hemi- 
plegia patient  moves  sideways  towards  the  paralysed  side  well, 
but  badly  towards  the  healthy  side,  so  that  in  right-sided  hemi- 
plegia the  patient,  when  going  sideways  towards  the  right  moves 
normally,  but  when  going  towards  the  left  he  drags  his  right 
leg  in  the  movement  of  adduction.  This  difference  in  the  side- 
gait  on  the  two  sides  in  organic  hemiplegia  is  often  quite  evident 
when  the  forward  gait  shows  very  Uttle  abnormality.  To  show 
the  phenomenon  properly,  the  patient  must  not  be  too  severely 


Fig.  140. — Gait  in  a  case  of  liysterical  monoplegia  of  right  leg. 

paralysed  to  stand  or  walk,  nor  must  he  have  shortening  of  the 
limb,  as  in  old  infantile  hemiplegia.  These  two  exceptions,  how- 
ever, are  readily  recognised  by  other  signs.  In  hysterical  hemi- 
plegia the  side-gait  is  impaired  on  both  sides,  not  merely  on 
the  healthy  side. 

An  ataxic  gait  is  seen  most  typically  in  tabes  dorsahs ;  but  it 
occurs  also  to  a  lesser  degree  in  other  diseases  imphcating  the 
posterior  columns  of  the  cord — for  example,  in  Friedreich's  ataxia, 
in  chronic  meningo-myelitis,  or  in  tumours  of  the  posterior  columns, 
also  in  ataxic  paraplegia  or  postero-lateral  sclerosis,  whether  due 
to  disseminated  sclerosis  or  to  other  causes.      Of  all  these,  the 


POSTUKES    AND    GAITS  285 

tabetic  gait  is  the  most  characteristic.  In  this  there  is  no  motor 
weakness  of  the  Hmbs,  but  they  are  characteristically  unsteady. 
The  patient  walks  on  too  broad  a  base,  with  his  legs  unduly  wide 
apart.  He  hfts  them  suddenly  and  violently,  raising  them  too  high, 
then  bangs  them  down  forcibly  in  flail-like  fashion,  stamping  the 
heels  on  the  ground.  He  tries  to  guide  his  tottering  course  by 
watching  the  ground.  Therefore  if  his  eyes  be  shut,  or  if  he 
be  in  the  dark,  and  especially  if  he  narrows  his  base  by  placing 
the  feet  close  together,  he  tends  to  fall.  In  slight  cases  of  tabetic 
ataxia,  when  the  patient  is  in  this  position,  he  may  not  actually 
fall,  but  we  can  see  the  tendons  on  the  dorsum  of  the  feet  actively 
in  movement,  in  the  eifoii;  to  preserve  the  balance.  With  this  gait 
we  usually  have  absence  of  the  knee-  and  ankle-jerks,  Argyll- 
Robertson  pupils,  and  various  other  signs,  such  as  lightning  pains, 
anfesthesige,  crises,  and  lymphocytosis  of  the  cerebro-spinal  jfluid.  In 
Friedreich's  ataxia  the  patient  is  commonly  an  adolescent,  and 
though  the  knee-  and  ankle-jerks  are  absent,  as  in  tabes,  the  pupils 
react  normally,  there  are  no  lightning  pains  nor  crises,  and  we 
usually  find  nystagmus,  scoliosis,  pes  cavus,  and  a  peculiar  affec- 
tion of  articulation.  In  ataxic  paraplegia  or  postero-lateral  sclerosis, 
where  the  lateral  columns  are  implicated  as  well  as  the  posterior, 
the  patient  is  ataxic,  but  with  increased  knee-jerks,  possibly 
ankle-clonus,  and  usually  an  extensor  type  of  plantar  reflex. 

A  reeling  or  titubating  gait  is  one  of  the  commonest  signs  of 
cerebellar  disease,  although  it  is  also  met  with  in  severe  vertigo 
of  any  variety,  whether  from  alcoholic  intoxication,  from  ear 
disease,  from  diplopia,  or  other  cause.  In  cerebellar  disease  the 
patient  staggers  along,  with  an  occasional  sudden  lurch  to  one 
or  other  side,  but  neither  lifting  his  feet  too  high  nor  stamping 
them  down,  as  in  tabes.  Not  uncommonly  the  cerebellar  patient 
has  a  tendency  to  stagger  persistently  in  some  particular  direction, 
depending  on  the  position  of  the  cerebellar  lesion — thus  he  may 
tend  to  fall  forwards,  backwards,  or  to  one  side.  As  a  rule,  he 
manages  to  pidl  himself  up  after  he  has  deviated  one  or  two  steps 
fi'om  his  straight  course.  In  some  cases  of  unilateral  tumour  of  the 
cerebellum  the  posture  of  the  head  is  altered,  the  ear  being  tilted 


286 


NERVOUS  DISEASES 


towards  the  shoulder  on  the  side  opposite  to  the  lesion,  and  the 
face  turned  shghtly  in  the  reverse  direction,  i.e.  towards  the  side 
of  the  lesion.  This  is  well  seen  in  Fig.  141,  which  represents  a 
woman  who  had  a  tumour  originating  from  the  meninges  over  the 
right  petrous  bone,  and  invading  the  right  lateral  lobe  of  the 
cerebelhim.  This  growth  was  successfully  localised  and  removed, 
but  the  patient  unfortunately  died  shortly  after.     This  "  cerebellar 


Fig.  141. — Case  of  right-sided  cerebellar  tumour  arising  from 
meningeal  sheath  of  auditory  nerve. 

attitude,"  however,  although  common  in  lateral  lobe  tumours,  is 
not  constant  in  its  direction.  For  example,  cases  have  been 
recorded  where  the  lateral  tilting  of  the  head  was  towards  the 
side  of  the  lesion,  and  the  rotation  of  the  face  to  the  opposite 
side.  Possibly  these  differences  are  associated  with  the  intra- 
or  extra-cerebellar  origin  of  the  growth. 

A  high- stepping  gait  occurs  in  patients  who  have  foot-drop. 
Such  a  patient,  to  clear  his  foot  from  the  ground,  lifts  the  leg 
too  high,  flinging  the  ankle  up  as  it  were,  instead  of  actively 
dorsiflexing  it.     This  gait  occurs  typically  in  peripheral  neuritis, 


POSTUEES  AND    GAITS 


287 


f^' 


also  in  muscular  dystrophies,  and  occasionally  in  lesions  of  the 
Cauda  equina  or  lower  part  of  the  lumbosacral  region  of  the  spinal 
cord.  It  also  occurs  unilaterally  in  paralysis  of  the  external  pop- 
liteal nerve.  The  gait  and  posture  of  muscular  dystrophy  also 
possess  other  characteristic  features.  Thus  from  weakness  of  the 
gluteal  muscles  the  patient  in  the  erect 
posture  arches  his  back,  in  order  to  keep 
the  hips  extended  (see  Fig.  142) ;  this  pro- 
duces lordosis  and  "  pot-belly."  Further, 
the  weakness  of  the  glutei,  as  already  ex- 
plained, causes  a  waddhng  gait,  the  legs 
being  planted  wide  apart ;  and  as  we  have 
already  seen,  the  mode  of  rising  from  the 
ground  in  such  cases  is  pathognomonic. 
Such  a  patient  when  placed  on  the  ground 
and  told  to  get  up  rolls  round  on  his  face, 
then  gets  on  his  hands  and  knees.  Then 
to  get  on  his  feet,  he  extends  the  knees, 
and  suddenly,  pressing  his  hands  on  one 
knee  after  the  other,  proceeds  to  extend 
the  hips  and  straighten  the  spine  by 
"  climbing  up "  his  own  thighs  until  he 
reaches  the  erect  posture. 

The  posture  and  gait  of  paralysis  agitans 
are  diagnostic,  so  much  so,  that  patients 
have  a  strong  family  resemblance  (see  Figs. 
143  and  144).  In  a  well-marked  case  the 
patient  stands  with  the  trunk  stooping 
forwards,  the  face  appearing  "  starched "  Fig.  142. 
and  expressionless — the  so-called  "  Parkin- 
sonian mask,"  in  which  there  is  httle  or 
no  emotional  play  of  features.  The  upper  limbs  are  slightly 
abducted  at  the  shoulders,  semi-flexed  at  the  elbows,  shghtly 
extended  at  the  wrists,  flexed  at  the  metacarpo -phalangeal  joints, 
and  extended  at  the  inter-phalangeal  joints,  as  if  holding  a 
pen — the  "  interosseal  "  attitude — and  very  often  they  show  the 


-Muscular  dys- 
trophy in  a  lad  of  17. 
Showing  lordosis. 


288  NERVOUS    DISEASES 

familiar  rhythmic,  "  pill-rolHng  "  tremor.  The  tremor  may  affect 
the  proximal  joints  as  well,  and  even  the  lower  limbs,  face,  jaw, 
palate  and  tongue.  All  the  voluntary  movements  of  the  trunk 
and  limbs  are  slow  and  stiff,  the  upper  limbs  no  longer  "swing" 
as  the  patient  walks  (in  unilateral  cases  this  loss  of  swing  is  con- 
fined to  the  arm  of  the  affected  side),  and  the  gait  is  "  festinant." 
The  patient  moves  forward  with  short,  shufffing  steps,  and  when  he 
turns,  his  trunk  moves  slowly  en  masse,  as  if  made  of  glass, 
whilst  his  steps  in  walking  tend  to  get  faster  and  faster,  as  if  he 


Fig.  143. — Paralysis  agitans — bilateral. 

were  "  chasing  his  own  centre  of  gravity."  This  is  called  "  pro- 
pulsion." Still  more  frequently  do  we  observe  "  retropulsion,"  in 
which  the  patient,  when  pulled  gently  from  behind,  tends  to  run 
backwards  with  short,  hasty  steps.  This  retropulsion  may  some- 
times be  induced  even  by  the  act  of  looking  upwards.  A  slighter 
degree  of  this  same  posture  and  gait  is  not  uncommon  in  simple 
old  age,  and  may  also  occur  in  pseudo-bulbar  paralysis  and  in 
the  multiple  lacunar  softenings  of  the  brain  described  by  Marie 
and  Ferrand. 

The  gait  in  chorea  is  sometimes  pecuUar,  partly  owing  to  a 
degree  of  ataxia,  partly  from  the  presence  of  additional  irregular 
involuntary  movements.     Sometimes  one  foot  seems  as  if  it  were 


POSTURES    AND    GAITS 


289 


momentarily  entangled  by  an  invisible  obstacle,  which  holds  the 
child  back  for  an  instant,  the  patient  then  hastily  resumes  his 
forward  progress ;  or  his  knee  may  give  way  suddenly,  causing 
him  to  fall. 

Many  chronic  epileptics  have  a  peculiar  slouching  posture  and 
gait,  the  posture  of  the  hands,  as  Spratling  ^  has  pointed  out, 
being  specially  characteristic.     The  fingers  are  habitually  flexed. 


Fig.  144. — Paralysis  agitans — bilateral. 

and   the   wrists   bent  to  a  right    angle,  and    the  patient  often 
has  a  marked  forward  stoop  of  the  shoulders. 

Various  deformities  produce  abnormalities  of  gait  and  posture. 
If,  for  example,  one  lower  limb  is  shortened  from  disease  of  the 
bones  or  joints,  from  malformations  such  as  coxa  vara,  or  con- 
genital dislocation  of  hip,  or  from  infantile  paralysis,  the  gait 
becomes  correspondingly  altered. 

1  New  York  Medical  Journal,  1905,  p,  849. 


CHAPTER    XVIII 

TROPHO-NEUEOSES 

The  central  nervous  system  exercises  a  profound  influence  on  the 
nutrition  of  all  the  tissues.  There  is,  however,  no  evidence  of 
the  existence  of  special  nerves  whose  function  is  trophic  and 
trophic  only.  The  control  over  nutrition  which  the  nervous  system 
possesses  is  probably  exercised  in  a  complex  fashion,  in  which 
there  are  several  factors  involved.  Striated  muscles,  for  example, 
undergo  atrophy  when  the  cells  of  the  corresponding  motor  nucleus 
in  the  cord  or  medulla  are  destroyed,  or  when  the  motor  nerve- 
fibre  leading  from  the  nerve-cell  to  the  muscle-fibre  is  interrupted. 
The  result  is  muscular  atrophy,  the  different  varieties  of  which  we 
have  already  studied  (see  p.  222).  Afferent  nerve-fibres  conveying 
sensory  impressions,  whether  conscious  or  subconscious,  have  also 
a  profound  influence  upon  tissue-nutrition,  especially  upon  that 
of  the  skin  and  its  appendages.  Therefore  in  anaesthetic  areas 
trivial  injuries  are  liable  to  produce  destructive  tissue-changes.^ 
Lastly,  the  central  nervous  system  indirectly  influences  the  tissues 
through  their  blood-supply,  by  means  of  its  connections  with  the 
sympathetic  vasomotor  system.  The  sympathetic  system  may 
also  be  disordered  primarily,  apart  from  the  central  nervous  system, 
not  only  in  gross  lesions  of  the  sympathetic  chain,  but  also  in 
the  so-called  angio-neuroses. 

Excluding,  then,  the  muscular  atrophies  and  the  angio-neuroses, 
which  are  studied  elsewhere,  let  us  direct  our  attention  to  certain 
trophic  disorders  which  are  associated  more  or  less  directly  with 
afiections  of  the  cerebro-spinal  nervous  system.  Trophic  disorders 
may  be  distributed  widely  all  over  the  body,  or  they  may  be 
limited  to  certain  circumscribed  areas  corresponding  to  a  peri- 
pheral nerve,  to  a  posterior  root,  or  to  some  division  of  the  spinal 
cord  or  brain. 


TROPHO-NEUROSES  291 

Generalised  Trophic  Disorders. — Of  these,  one  of  the  best 
examples  is  the  well-known  anorexia  nervosa.  In  this  affection, 
without  evidence  of  structural  disease  of  any  organ,  the  patient 
(generally  a  young  woman)  loses  appetite  and  becomes  pro- 
gressively emaciated,  often 'to  a  profound  degree.  The  condition 
sometimes  follows  a  shock,  physical  or  mental,  perhaps  an  affaire 
du  coeur,  though  in  other  instances  we  can  find  no  apparent 
exciting  cause.  In  diagnosing  this  condition,  we  have  first  to 
exclude  other  conditions,  such  as  diabetes,  tuberculosis,  and 
malignant  disease,  which  commonly  produce  emaciation.  The 
patient  generally  exhibits  certain  "  stigmata  "  of  functional  disease. 
Of  these  stigmata  the  most  frequent  is  a  hemi-ansesthesia,  usually 
slight  in  degree  and  generally  left-sided  (see  later,  p.  368). 

In  marked  contrast  to  this  is  the  rare  afiection  known  as 
adiposis  dolorosa,  or  Dercum's  disease.  It  occurs  chiefly  in  middle- 
aged  women,  many  of  the  patients  being  alcoholic  or  syphilitic. 
The  patient  is  diffusely  obese,  and,  in  addition,  she  has  localised 
fatty  lumps  in  the  subcutaneous  tissue,  forming  large  pendulous 
swellings,  chiefly  on  the  limbs  and  trunk.  These  swellings  may 
be  symmetrical  or  asymmetrical.  They  appear  and  steadily 
increase  in  size,  consisting  of  fat  and  of  an  embryonic  form  of 
connective  tissue.  The  arms  are  most  frequently  the  sites  of 
the  swellings,  which  are  usually  tender  on  pressure  and  may 
have  spontaneous  pains.  Certain  areas,  however,  such  as  the 
hands,  feet,  and  face,  are  always  spared.  The  nerve-trunks  are 
tender,  and  there  may  be  areas  of  blunting  or  loss  of  cutaneous 
sensibility.  Sometimes  the  thyroid  and  pituitary  glands  are 
indurated,  but  the  patient  has  none  of  the  mental  or  physical 
features  of  myx oedema. 

A  curious  condition  of  the  bones  results  from  hjrpertrophy  or 
functional  over-activity  of  the  anterior  lobe  of  the  pituitary  gland. ^ 

1  Acromegaly  cannot  be  ascribed,  as  was  formerly  thought,  to  deficient 
pituitary  secretion,  for  as  Tamburini  and  Modena  have  pointed  out  {Rivista 
sperimentale  di  Freniatria,  1903,  fasc.  3  and  4),  experimental  destruction  of 
the  gland  does  not  cause  acromegaly,  nor  do  malignant  growths,  nor  tuber- 
culous disease  of  the  gland  produce  it,  but  only  conditions  such  as  hyper- 
trophy or  adenoma. 


292 


NERVOUS    DISEASES 


Hyper-secretion  by  this  gland  appears  to  set  free  in  .the  body  certain 
abnormal  substances  whose  action  is  to  cause  an  extraordinary 
growth  of  bony  tissues.  If  the  disease  sets  in  before  the  age  at 
which  the  epiphyses  have  become  joined,  the  bones  grow  enormously 
in  all  their  dimensions,  and  the  result  is  gigantism.       But   if  the 


Fia    145. 


Fig.  146. 


Acromegaly  of  eight  years'  duration  in  a  man  aged  42. 
had  bi-temporal  hemianopia. 


The  patient 


affection  begins  after  the  epiphyses  have  united,  the  overgrowth 
of  the  bones  is  confined  to  their  ends,  producing  acromegaly. 

The  phenomena  of  acromegaly  are  very  characteristic  (see 
Figs.  145  and  146).  There  is  a  progressive  enlargement  of  the 
bones  and  soft  parts,  most  marked  in  the  hands  and  feet,  but 
also  affecting  other  parts,  notably  the  skull  and  face.     The  skull 


TROPHO-NEUROSES  293 

becomes  enlarged  and  thickened,  all  its  bony  ridges  are  ex- 
aggerated ;  the  margins  of  the  orbits,  the  cheek-bones,  and  most 
striking  of  all,  the  lower  jaw,  become  enlarged.  The  mandible 
becomes  prognathous,  the  lower  teeth  biting  in  front  of  the 
upper,  instead  of  vice  versa,  and  the  teeth  become  widely  separ- 
ated. The  soft  parts  also  share  in  the  hypertrophy.  The  lower 
lip,  the  tongue,  uvula,  tonsils,  and  the  cartilages  of  the  ears,  all 
become  enlarged,  and  the  skin  of  the  face  becomes  thick  and  coarse. 
The  hands  and  feet  increase  in  size  (not  the  nails),  so  that  the 
patient  requires  gloves  and  shoes  several  sizes  larger  than  before. 
Spinal  curvature  is  also  present,  usually  a  cervical  kyphosis,  and 
the  thorax,  pelvis,  and  even  the  external  genitals  become  enlarged. 
Glycosuria  is  a  fairly  common  comphcation.  In  female  patients 
amenorrhoea  occurs.  In  addition  to  these  phenomena  the  patient 
complains  of  severe  headaches,  owing  to  the  intra-cranial  pituitary 
tumour.  This  tumour,  from  its  position  in  the  sella  turcica,  fre- 
quently encroaches  on  the  adjacent  optic  chiasma,  and  then  there 
is  produced  a  corresponding  affection  of  the  visual  fields  (see  p.  124) 
usually  commencing  as  a  bi-temporal  hemianopia,  which  may,  as 
the  disease  advances,  progress  to  complete  blindness. 

Apart,  however,  from  pituitary  disease,  which  strictly  speak- 
ing, although  intra-cranial,  is  not  primarily  a  nervous  disorder, 
we  sometimes  have  widespread  overgrowth  of  the  tissues,  confined 
to  one-half  of  the  body  and  probably  of  cerebral  origin.  Fig.  147 
represents  such  a  patient  with  left-sided  hemi-hypertrophy,  in  whom 
all  the  bones  of  the  left  side  (as  verified  by  skiagrams),  including 
those  of  the  face,  hmbs,  pelvis  and  thorax,  together  with  the  soft 
tissues  of  the  face,  tonsil,  tongue  and  testicle,  were  larger  than 
on  the  right  side.  But  the  right  side  of  the  cranium,  and  pro- 
bably also  the  right  side  of  the  brain,  were  larger  than  the  left. 

Passing  next  to  trophic  disorders  of  more  hmited  distribution, 
it  is  convenient  to  discuss  them  in  certain  groups. 

Bilateral  thrombosis  of  the  arteries  of  the  corpora  striata,  and 
especially  of  the  lenticular  nuclei — a  not  uncommon  occurrence 
in  fatal  poisoning  by  sewer  gas — ^produces  what  Dana  ^  has  called 

^  Journal  of  Nervous  and  Mental  Disease,  1908,  p.  65. 


291 


NERVOUS  DISEASES 


the  "  corpus  striatum  syndrome,^'  in  which,  in  addition  to  coma 
(with  perhaps  hemiplegia  or  diplegia  from  affection  of  the  ad- 
jacent pyramidal  paths),  there  is  a  gangrenous  condition  of  the 
skin  and  sometimes  of  the  lungs  as  well. 

Trophic  Changes  in  the  Skin  and  its  Appendages. — Glossy 


Fig.  147. — Left-sided  hemi-hypertrophy. 

skin  is  a  condition  met  with  chiefly  in  the  hands,  in  certain  cases 
of  long-standing  peripheral  nerve  palsies,  whether  traumatic  or 
neuritic  in  origin.  It  is  also  a  frequent  accompaniment  of  osteo- 
arthritis, not  only  in  the  ordinary  "  rheumatoid  "  variety,  but  also 
in  the  arthritis  which  comes  on  in  hemiplegic  limbs.  The  skin 
of  the  fingers  becomes  thinned  and  atrophic,  with  a  peculiar  smooth, 
shiny  surface.  The  nails  in  many  cases  are  altered,  being  longi- 
tudinally striated  and  excessively  curved  from  side  to  side.     The 


TROPHO -NEUROSES  295 

finger-pads  are  wasted  and  the  finger-tips  taper  to  a  point,  as  is 
seen  in  Fig.  148,  which  is  taken  from  a  case  of  right-sided  brachial 
neuritis. 

Perforating  ulcers  occur  most  typically  in  tabes  dorsalis.  They 
are  generally  situated  on  the  foot,  on  its  plantar  surface,  especially 
at  the  metatarso-phalangeal  joint  of  the  great  or  httle  toe.  They 
may  also  occur  under  the  heel  or  under  the  terminal  phalanx  of 
the  hallux.  Each  ulcer  begins  as  a  thickening  of  the  epidermis, 
like  a  corn.     Suppuration  occurs  under   this,   and  the  pus  finds 


Fig.  148. — Right-sided  brachial  neuritis  with  glossy  skin  and  tapering  finger-tips. 

its  way  out  through  a  small  opening  in  the  centre  (Fig.  149). 
A  narrow  sinus  is  thus  formed  which  increases  in  depth  until  it 
may  extend  into  the  joint  beneath,  which  is  often  disorganised., 
and  carious  bone  may  be  felt  at  the  bottom.  Sometimes  the  ulcer 
heals  up  under  treatment.  The  tabetic  perforating  ulcer  is  pain- 
less. Somewhat  similar  trophic  ulcers  are  met  with  in  certain 
cases  of  sfina  bifida  occulta  and  also  in  syringomyelia,  but  in  this 
latter  disease  they  are  commoner  in  the  hands.  Diabetic  neuritis 
is  also  occasionally  associated  with  perforating  ulcers  of  the  feet, 
a  minor  variety  of  diabetic  gangrene.  In  leprous  neuritis  per- 
forating  ulcers    are   not   infrequent,   though  it    is    commoner   to 


296 


NERVOUS    DISEASES 


have  a  still  more  extensive  loss  of  tissue,  whole  phalanges 
dropping  from  the  fingers  and  toes.  Painless  whitlows — ^in  so- 
called  "  Morvan's  disease,"  a  sub-variety  of  syringomyelia,  are 
found  at  the  finger-tips.  These  whitlows  are  sometimes  the  result 
of  trivial  injuries  which  in  a  normal  individual  would  not  produce 
any  serious  results.  In  other  cases  the  explanation  is  found  in 
the   absence   of    sensibility   to   temperature   and   pain,   which   is 


Fig.  149. — Perforating  ulcers  in  tabes. 

characteristic  of  the  disease,  so  that  the  patient  burns  the  fingers 
painlessly  and  produces  blisters  and  even  areas  of  sloughing. 

In  certain  cases  of  tabes  there  may  be  a  perforating  ulcer  in 
the  mouth.  First  the  teeth  become  loosened  and  fall  out,  then 
the  alveolar  margin  of  the  jaw  is  absorbed,  and  if  the  upper  jaw 
be  affected  a  perforation  into  the  nasal  cavity  may  be  established. 

Herpes  zoster  is  a  very  typical  example  of  a  trophic  cutaneous 
disorder  which  has  a  direct  nervous  origin,  viz.,  inflammation  or 


TROPHO-NEUROSES 


297 


thrombosis  of  the  corresponding  posterior  root  gangUon.  In  this 
affection  a  crop  of  vesicles  appear,  which  are  distributed  in  a 
definite  metameric  area,  corresponding  to  the  posterior  root 
whose  ganghon  is  diseased.  In  the  case  of  facial  herpes  it  is  the 
Gasserian  ganglion  which  is  inflamed,  in  whole  or  in  part,  whilst 
herpes   of    the    external   auditory   canal    is    associated   with   in- 


FIG.  150. 

Herpes  zoster  in  area  of  fifth 
dorsal  root.  Second  day  after 
appearance  of  eruption. 


Herpes  zoster — the  same  patient  as  in 
Fig.  150.  Eruption  surrounds  the 
nipple,  and  thence  extends  inwards 
to  mid-sternum. 


flammation  of  the  geniculate  ganglion.  The  herpetic  vesicles 
usually  become  pustular  and  subsequently  permanent  scars  may 
remain.  Herpes  is  sometimes  preceded,  for  a  day  or  two,  by  pre- 
herpetic  pain  in  the  area  where  the  eruption  is  about  to  appear ; 
and  not  infrequently  the  eruption  is  followed  by  prolonged  and 
intractable  post-herpetic  neuralgia.  Figs.  150  and  151  are  from  a 
typical  case  of  herpes  in  the  area  of  the  fifth  thoracic  root. 
Sometimes    herpes    develops   in    the    course    of    diseases    of   the 


298  NERVOUS    DISEASES 

vertebrse  or  of  the  spinal  meninges.  Such,  an  occurrence  signifies 
that  the  morbid  process  has  attacked  the  corresponding  posterior 
root  ganghon  or  ganglia.  Even  in  simple  herpes  zoster  we  can 
sometimes  elicit  Kernig's  sign-^  (see  p.  60). 

Bed-sores  result  from  inflammatory  and  destructive  changes  in 
the  skin  and  underlying  tissues  of  bedridden  patients,  whether  in 
cases  merely  enfeebled  by  prolonged  illness  (especially  in  enteric 
fever)  or,  more  commonly,  in  severe  organic  paralysis,  such  as 
hemiplegia  or  paraplegia.  Most  bed-sores,  occurring  as  they  do 
at  the  sites  of  pressure,  can  be  prevented  by  careful  nursing,  by 
keeping  the  patient's  skin  scrupulously  clean  and  dry,  by  placing 
him  on  a  water-bed,  and  by  hardening  the  epidermis  by  local 
applications  of  methylated  spirit.  But  sometimes  in  spite  of  the 
most  assiduous  nursing,  bed-sores  may  develop  mthin  a  few  days 
or  even  within  a  few  hours  of  an  initial  paraplegia  or  hemiplegia. 
This  so-called  acute  decubitus  is  of  grave  omen. 

The  commonest  site  for  a  bed-sore  in  a  hemiplegic  patient  is 
over  the  great  trochanter  on  the  paralysed  side.  In  paraplegia 
from  cord  lesions,  e.g.  acute  myelitis,  the  bed-sore  commonly  forms 
over  the  middle  of  the  sacrum  (Fig.  152).  A  bed-sore  commences 
as  an  area  of  redness  of  the  skin,  bullse  then  develop  and  burst, 
leaving  an  ulcerating  or  sloughing  surface  beneath.  The  sloughing 
process  may  extend  down  to  the  periosteum  and  bones,  and  in 
sacral  decubitus  the  infection  may  extend  into  the  vertebral 
canal,  producing  a  fatal  cerebro-spinal  meningitis,  septic  organisms 
gaining  access  not  only  from  the  skin,  but  from  the  intestinal  dis- 
charges. Bed-sores  are  also  met  with  in  advanced  cases  of 
bedridden  dementia,  even  where  there  is  no  paralysis.  In  these 
patients,  as  in  cases  of  prolonged  fever,  the  sores  develop  on 
the  pressure  points,  viz.  the  heels,  hips,  backs  of  the  scapulae 
and  even  on  the  inner  sides  of  the  knees.  We  also  meet  with 
excoriations    of   the   skin,   which   may   amount  to   bed-sores,    in 

1  This  fact,  together  with  the  freqvient  occurrence  of  lymphocytosis  of  the 
cerebro-spinal  fluid,  shows  that  in  herpes  zoster  the  pathologica,!  process  is  not 
necessarily  limited  to  the  posterior  root-ganglion,  but  is  part  of  a  more  widely 
diffused  meningeal  irritation. 

Bilbeza,  Archives  generales  de  Med.,  Feb.  27,  1906. 


TROPHO-NEUEOSES 


299 


cases    of    violent    chorea,   where   the   patient    knocks    his    limbs 
against  surrounding  objects. 

Before  leaving  the  subject  of  destructive  trophic  lesions  of  the 
skin,  we  must  mention  symmetrical  gangrene,  a  localised  gangrene 


l"lG.  152. — Lurubo-sacral  myelitis  with  sacral  bed-sore  or  decubitus. 
Showing  atrophy  and  paralysis  of  muscles  below  left  knee.  The 
small  chart  on  the  right  indicates  the  coexisting  area  of  antesthesia. 

chiefly  occurring  in  the  tips  of  the  fingers  and  toes,  and  preceded 
by  pains  or  para3sthesi8e  of  the  parts.  But  to  this,  the  most  severe 
phase  of  Raynaud's  disease,  we  shall  refer  again  when  we  con- 
sider the  angio-neuroses. 

The  commonest  points  of  incidence  of  rodent  ulcers,  especially 


300  NERVOUS   DISEASES 

on  the  face,  as  Cheatle  ^  has  shown,  are  at  the  positions  where 
the  various  branches  of  the  trigeminal  nerve  become  cutaneous, 
especially  over  the  points  of  emergence  of  the  infra-orbital,  infra- 
trochlear,  temporo-malar  and  lachrymal  nerves,  and  also  with 
particular  frequency  at  the  inner  canthus  of  the  eye  and  at  the 
angle  where  the  ala  nasi  joins  the  cheek.  He  has  also  shown 
that  these  spots  are  the  favourite  points  of  incidence  of 
leucoderma  and  scleroderma.  The  precise  significance  of  these 
facts  is  still  obscure,  but  Cheatle  has  recorded  the  curious  fact 
that  rodent  ulcers  are  frequently  limited  to  the  distribation  of 
normal  nerve-areas  and  that  the  spread  of  a  rodent  ulcer  ceases 
abruptly  when  it  reaches  a  cutaneous  area  which  has  become 
denervated  by  division  of  its  sensory  nerves. 

There  are  other  trophic  lesions  unaccompanied  by  necrosis  or 
ulceration,  and  consisting  in  local  changes  affecting  one  or  more  ele- 
ments of  the  skin  or  subcutaneous  tissues,  whether  in  the  direction 
of  atrophy  or  of  hypertrophy.  Perhaps  the  most  typical  examples 
of  this  variety  are  scleroderma,  leucoderma,  and  cutaneous  naevi. 
Scleroderma  is  a  disease  in  which  the  skin  becomes  abnormally  hard 
and  fibrous.  The  condition  may  be  diffuse  or  circumscribed.  In 
the  rarer  diffuse  variety,  large  areas  of  skin,  usually  symmetrical, 
and  especially  in  the  upper  limbs,  become  hard  and  rigid,  losing 
their  elasticity  so  that  the  affected  skin  can  no  longer  be  pinched 
up  with  the  fingers.  Sometimes  there  is  a  prehminary  oedematous 
stage.  As  the  disease  advances,  the  sclerotic  process  may  extend 
to  deeper  structures  such  as  tendons,  and  this,  with  the  rigidity  of 
the  skin,  hmits  the  movements  of  the  joints  and  may  produce 
permanent  deformities.  If  the  fingers  are  affected,  they  become 
tapering  at  the  tips  and  permanently  flexed.  If  the  face  is  affected, 
it  becomes  immobile  and  mask-like.  Circumscribed  scleroderma,  or 
morphoea,  is  the  commoner  variety,  where  small  patches  of  skin 
become  hard,  white  and  ivory-like,  the  distribution  of  the  patches 
being  somewhat  similar  to  those  of  herpes  zoster — i.e.  meta- 
merically,  in  the  area  of  a  posterior  root,  or  of  one  of  the  divisions 
of  the  trigeminal  nerve  on  the  face. 

1  Brit.  Med.  Journal,  April  29.  1905. 


TROPHO-NEUROSES 


301 


Leucoderma,  or  disappearance'^of  pigment  from  circumscribed 
patches  of  skin,  is  also  commonly  distributed,  more  or  less, 
in  nerve-areas.  The  patch  of  absolute  pallor  has  a  pigmented 
edge  where  it  joins  the  normal  skin,  and  it  tends  to  spread 
slowly  along  the  particular  area.  This  disease,  of  course,  is  most 
striking  when  it  affects  patients  of  sallow  complexion  or  of  dark- 


FlG.  153.  I'IG.  154. 

Congenital  verrucosis  of  metameric  distribution. 

skinned  race.  Leucoderma  also  occurs  in  the  maculo-ansesthetic 
type  of  leprosy,  where  the  leucodermic  patches  are  often  red  and 
hypereesthetic  at  the  edges  and  anaesthetic  in  the  centre. 

Figs.  153  and  154  represent  a  little  girl  aged  eight,  in  whom 
patches  of  warty  growths  were  distributed  metamerically  on  the 
limbs  and  trunk. 

Congenital  cutaneous  ncevi — "  port-wine  stains  " — are  also  com- 
monly distributed  in  root  areas  on  the  trunk  or  in  the  trigeminal 


302 


NERVOUS   DISEASES 


distribution  on  the  face.  Tlie  trigeminal  area  is  affected  with 
special  frequency,  one,  two,  or  all  three  divisions  of  the  trigeminal 
being  mapped  out,  more  or  less  accurately.  It  is  an  interesting 
fact  that  a  cutaneous  nsevus  on  the  face  may  be  associated 
with  hypertrophy  of  the  subjacent  deep  tissues,  with  enlargement 
of     the    eyeball,    and    even    with    a     nsevoid    condition    of    the 


Fig.  155.  Fig.  156. 

von  Recklinghausen's  disease  in  a  man  aged  38. 

nasal  mucous  membrane  and  of  the  dura  mater  on  the  correspond- 
ing side,  all  of  which  structures  are  innervated  by  the  trigeminal 
nerve.  More  than  this,  cases  of  nsevus  of  the  face  may  be  asso- 
ciated with  recurrent  epistaxis  from  the  nsevoid  nasal  mucosa,  and 
sometimes  they  develop  sudden  infantile  hemiplegia  with  epilepti- 
form convulsions,  due  to  sub-dural  haemorrhage  from  the  dural 


nsevus. 


Gushing,  Journal  of  American  Med.  Association,  1906,  p.  178. 


TROPHO-NEUROSES 


303 


Large  neuro-fibromata— so-called  'plexiform  neuroma  or  ele- 
phantiasis  nervorum — are  more  common  on  the  trigeminal  nerve, 
especially  in  its  upper  divisions,  than  on  any  other  nerve  of  the 
body.  Such  a  tumour  is  generally  part  of  a  more  widespread 
affection  known  as  von  Reddinghausen'' s  disease  (see  Figs.  155,  156). 
In  this  disease  we  find,  in  a  complete  case,  neuro-fibromata,  often 
of  fairly  large  size,  forming  painless  swellings  on  the  face  or  else- 
where, together  with  multiple  soft  fibromata  forming  sessile  or 
pedunculated  growths  (known  as  molluscum  fibrosum)  and  also 
patches  of  cutaneous  pigmentation  distributed  more  or  less  de- 
finitely in  nerve  areas.     The  neuro-fibromata   of  von  Reckling- 


Fig.  157. — Case  of  tabes  with  loss  of  hair  in  area  of  L5  and  Sj  roots. 
hausen's  disease  do  not  cause  symptoms  except  by  accidental 
mechanical  compression  of  adjacent  structures.  The  disease  often 
appears  in  childhood  and  remains  stationary  for  many  years,  when 
it  may  suddenly  resume  its  spread,  new  tumours  cropping  out  all 
over  the  body. 

Various  cutaneous  lesions  are  present  in  many  cases  of  arsenical 
neuritis.  A  brownish  macular  pigmentation  of  the  skin  is,  of 
course,  common  in  chronic  arsenical  poisoning,  without  neuritis. 
But  in  arsenical  neuritis  we  frequently  observe  special  cutaneous 
affections,  such  as  glossy  skin,  herpes  zoster,  falling  of  the  hair, 
and  most  characteristic  of  all,  hyperkeratosis  of  the  palms  and 
soles,  where  the  epidermis  becomes  much  thickened  and  tends  to 
desquamate.  In  addition  to  these  skin  lesions,  we  have  the 
ordinary  signs  of  a  peripheral  neuritis,  such  as  drop-wrist,  drop- 
foot,  &c. 


■ji.iil  .  ..Ll3  .GJ'gDiquirt,.!  iioj  '  ..   ailanoai 


^ 


c 


TROPHO-NEUROSES  305 

in  other  nerve-areas.  The  hair  may  also  be  affected  in  various  ways 
in  other  nervous  affections.  Well- authenticated  cases  have  been 
recorded  of  blanching  of  the  hair  of  the  scalp  within  a  few  hours, 
as  a  result  of  profound  emotion.  It  is  not  uncommon  to  meet 
with  patches  of  whitened  hair  in  nerve-areas  which  have  been 
the  site  of  severe  neuralgia.  Even  in  the  ordinary  greyness  of 
advancing   years,  and  in   the  idiopathic    premature    greyness   of 


Fig.  159.  Fig.  16U. 

Eight-sided  facial  hemiatrophy,  also  implicating  the  corresponding  side 
of  the  tongue. 

youth,  as  Cheatle  ^  has  pointed  out,  the  maximum  greyness 
often  appears  in  nerve-areas  in  the  scalp  and  beard.  There  is 
a  variety  of  localised  alopecia  where  the  hair  falls  out  suddenly 
in  a  certain  nerve  area.  Fig.  157  is  from  a  case  of  tabes  where 
there  was  a  curious  absence  of  hair  in  certain  root-areas  in  the 
legs.  Many  cases  of  exophthalmic  goitre,  as  Walsh  pointed  out,^ 
have  a  band  of   alopecia  at  the  frontal  end  of  the  scalp.     We 

1  Brit.  Med.  Journal,  July  22,  1905. 
-  Lancet,  1907,  p.  1080. 


306 


NEEVOUS   DISEASES 


occasionally  meet  with  cases  of  universal  alopecia,  where  the  hairs 
all  over  the  body  fall  out,  and  the  patient  may  remain  perma- 
nently hairless,  his  skin  meanwhile  being  considerably  thinned. 

Trophic  changes  in  the  nails  occur  in  a  number  of  nervous 
diseases.  Sometimes  the  nails  become  hypertrophied,  as  in 
the  toe-nails  of  patients  with  chronic  paraplegia  from  any  cause. 
In   peripheral  neuritis,  especially  the    arsenical   variety,    we    may 


Fig.  161. — Hemi-bypertrophy  of  right  side  of  face. 

meet  with  excessive  curving,  brittleness,  atrophy  and  even  falhng 
of  the  nails.  In  tabes  the  toe-nails,  especially  those  of  the  big  toes, 
are  sometimes  shed,  whilst  in  some  cases  of  cerebral  haemorrhage  we 
find  haemorrhages  under  the  nails  of  the  hemiplegic  hand  (Fig. 
158  and  Plate  I.).  As  the  nail  grows,  the  hsemorrhagic  area 
is  gradually  cast  off. 

Trophic  Changes  in  Bones  and  Joints. — An  affection  which 
possesses  characters  common  to  this  group  and  to  the  group  of 
cutaneous  trophic  lesions  is  progressive  facial  hemiatrophy.      It  is 


TROPHO-NEUROSES 


307 


probably  referable,  as  we  have  already  seen,  to  a  lesion  of 
the  trigeminal  nerve  or  nucleus.  Not  only  is  the  skin  on  the 
affected  side  of  the  face  atrophied  and  wrinkled,  but  the  bones, 
and  especially  the  lower  jaw,  become  smaller  (Figs.  159  and  160). 


Fig.  1()2. — Old  infantile  hemiplegia, 
left-sided,  with  arrested  growth  of 
limbs. 


Fig.  1G.3. — Old  poliom3'eliiis  anterior 
acuta.  Paralysis  and  atrophy  of  bicep.«, 
triceps,  and  deltoid  on  left  side,  with 
arrested  growth  of  humeiiis. 


Still  more  rarely,  we  meet  with  cases  of  facial  hemi-hypertro'phy, 
where  the  bones  and  soft  parts  of  one  side  of  the  face  become  pro- 
gressively larger.  In  the  case  shown  in  Fig.  161,  the  enlargement 
of  the  face  followed  an  injury  to  the  forehead  in  childhood  on 
the  side  which  afterwards  became  enlarged. 

It  is  not  uncommon  to  find  atrophic  changes  in  the  bones  of 
paralysed  hmbs.     In  paralytic  affections  of  children,  whether  of 


308 


NERVOUS    DISEASES 


the  upper  neurone  type,  as  in  infantile  hemiplegia  (Fig.  162),  or  of 
the  lower  neurone  type,  as  in  acute  anterior  poliomyelitis  (Fig.  163), 
the  bones  of  the  paralysed  limb  become  arrested  in  their  growth 
and  are  smaller  in  all  their  dimensions  than  are  the  healthy  hmbs. 
Even  in   some   cases   of   hemiplegia   in  adults   the   bones  of  the 


Fig.  164. — Tabetic  arthropathy  of  both  knees  and  of  right  foot.     The  patient's 
right  leg  is  tied  to  the  chair  to  prevent  involuntary  tabetic  movements. 

paralysed  Hmbs  become  excessively  brittle.  I  remember  a  case 
of  hemiplegia  in  a  middle-aged  woman  where  moderate  passive 
movements  under  an  anaesthetic,  during  an  attempt  to  break  down 
adhesions  in  the  hip-joint  of  the  hemiplegic  side,  caused  a  fracture 
of  the  neck  of  the  femur.  The  brittleness  of  the  bones  in  certain 
insane  patients  and  their  liability  to  fractures  on  trivial  injuries 
are    well  known.     Moreover,   there    is  a   rare  disease   known    as 


TROPHO-NEUROSES  309 

idiopathic  jragiliias  ossium,  where  the  patient,  otherwise  healthy, 
may  fracture  his  bones  from  minimal  accidents,  as,  for  example, 
where  a  lad  fractured  his  humerus  by  throwing  a  cricket-ball. 
Similar  spontaneous  fractures  also  occur  in  certain  cases  of  tabes 
and  of  syringomyelia,  but  in  these  two  diseases  the  fractures  are 


^ 


Fig.  165. — Syringomyelia  with  arthropathy  of  left  shoulder-joint. 
Atrophy  of  intrinsic  muscles  of  left  hand. 

painless,  so  that  the  patient  may  continue  to  use  the  fractured 
limb  in  a  fashion  impossible  to  a  normal  individual. 

Trophic  changes  in  joints — the  so-called  arthropathies,  are  met 
with  most  typically  in  tabes  (constituting  Charcot's  joint),  in 
syringomyeha,  and  in  some  cases  of  leprosy.  The  large  joints 
are  generally  those  afTected,  the  knee  and  the  tarso-metatarsal  joint 
being  the  joints  most  commonly  attacked  in  tabes  (Fig.  164),  the 
shoulder  in  syringomyeha  (Figs.  165  to  168).      But  in  tabes  even 


310 


NERV(3US   DISEASES 


the  smaller  joints  may  occasionally  be  affected,  as  in  the  patient 
shown  in  Fig.  166,  where  the  terminal  joint  of  the  thumb  was  thus 


Fig.  166.— The  same  case  of  syringomyelia.     Showing  the  area  of 
therm-ansesthesia  and  analgesia. 

diseased.  Female  tabetics  seem  to  be  relatively  more  liable  than 
male  patients  to  osteopathies  and  arthropathies.  The  exciting  cause 
of  a  tabetic  arthropathy  is  often  some  trivial  traumatism,  such  as 


Fig.  167.  —  Syringomyelia  (same  case  as  Fig.  165).  Eadiogram 
of  shoulder-joint.  Showing  fracture  of  upper  end  of  humerus, 
also  osteophytic  outgrowth  from  axillary  border  of  scapula. 


a  twist  or  sprain  in  a  joint  in  which  the  sense  of  pain  is  diminished 
or  lost,  hence  the  greater  frequency  of  tabetic  arthropathies 
in  the  lower  hmbs.  The  joint  swells  painlessly,  and  rapid  de- 
structive changes  occur  in  its  articular  surfaces,  which  become 
eroded  and  may  disappear,  together  with  a  considerable  part  of 
the  adjacent  bone.     Fractures  of  the  articular  ends  are  common, 


TROPHO-NEUEOSES 


311 


both   in    tabetic   and    in    syringomyelic  joints.      The    ligaments 
become  lax  and  the  joint   abnormally    mobile,  so,  that   in   the 


Fig.  168.— Syringomyelia  with  arthropathy  of  left  shoulder-joint,  the  limb 
being  swollen  and  displaced  downwards  "  en  masse  "  at  the  shoulder. 


Fig.  Ifi9. — Tabetic  arthropathy  of  left  thumb. 


312 


NERVOUS    DISEASES 


knee  we  may  be  able  to  produce  lateral  passive  movements, 
or  even  to  bend  the  joint  into  all  sorts  of  curious  positions 
(Fig.  170).  The  joint  is  sometimes  distended  with  a  glairy 
gelatinous  fluid,  which  may  be  blood-stained.  In  the  later  stages 
this  fluid  may  be  reabsorbed,  throwing  into  relief  the  deformity 
of  the  bones  (Fig.  171).  But  the  changes  in  such  arthropathies  are 
not  entirely  destructive.     Osteophytic  outgrowths  are  often  formed 


Fig.  170. — Tabetic  arthropathy  of  knee-joints. 

in  the  peri-articular  tissues,  causing  irregular  thickening  of  the 
bones,  and  producing  Httle  islands  of  new  bone  amongst  the 
tissues  around  the  joint.  These  can  be  readily  detected  on  palpa- 
tion and  verified  by  skiagrams  (Figs.  172  and  173). 

Joint  affections  of  a  different  kind  are  met  with  in  some  cases 
of  chronic  hemiplegia.  The  joints  of  the  paralysed  limbs,  two  or 
three  weeks    after   the   hemiplegic   attack,   become    swollen  and 


TKOPHO-NEUROSES 


313 


deformed.  But,  unlike  tlie  tabetic  and  syringomyelic  arthropatliies, 
hemiplegic  joint-afiections  are  acutely  painful.  Moreover,  the 
changes   in  hemiplegic   joints   are   not   destructive   but   more    of 


Fig.  171. — Syringomyelia  with  arthropathy  of  right  shoulder-joint,  and 
destruction  of  head  of  humerus.     Well-marked  scoliosis. 


Fig.  172. — Tabetic  arthropathy  of  elbow-joint.     Radiogram 
showing  bony  deposits  in  the  tissues  around  the  joint. 

the  nature  of    a  subacute  osteo-arthritis,  with  pain  and  rigidity 
on  passive  movements  and  with  a  tendency  to  the  formation  of 


314 


NEEVOUS   DISEASES 


fibrous  adhesions  within  the  joint  and  to  thickening  of  the 
joint  capsule.  When  the  fingers  are  affected,  they  lose  their 
normal  outline  and  become  clumsy-looking  and  "  sausagy "  in 
appearance.  Together  with  this  heroiplegic  arthritis  it  is  not 
uncommon  to  have  a  degree  of  muscular  wasting,  but  without 
electrical  reactions  of  degeneration. 

Finally,  we  must  bear  in  mind  that  certain  hysterical  patients 
complain  of  joint-pains,  usually  mono-articular,  which  may  more 


Fig.  173.— Radiogram  of  tabetic  arthropathy  of  knee,  from 
patient  shown  in  Fig.  164.  Showing  disappearance  of  articular 
surfaces  and  presence  of  bony  deposits  in  peri-articular  tissues. 

or  less  closely  simulate  organic  joint  disease.  The  patient  is 
commonly  a  young  woman  who,  after  some  local  injury  to  the 
joint,  or  after  some  emotion,  or  perhaps  from  being  acquainted 
with  another  patient  who  has  joint  disease,  suddenly  complains 
of  intense  joint-pain,  together  with  cutaneous  hyperaesthesia  in 
that  region.  The  joint  is  rigid  and  resistant  to  passive  move- 
ment, and  if  the  condition  has  persisted,  as  is  sometimes  the 
case,  for  weeks  or   months,  fibrous    adhesions    may  form.      But 


TKOPHO-NEUEOSES  315 

there  is  no  true  swelling  of  the  joint  when  compared  with  the 
corresponding  limb  of  the  opposite  side,  though  a  false  appearance 
of  swelling  may  appear  to  be  present  owing  to  disuse-atrophy  of 
the  adjacent  muscles.  The  presence  of  other  hysterical  "  stigmata  " 
often  aids  in  the  diagnosis,  but  an  accurate  opinion  is  sometimes 
a  matter  of  considerable  difficulty  and  is  arrived  at  by  a  pro- 
cess of  exclusion.  Accomplished  surgeons  have  been  known  to 
operate  on  such  joints  and  only  on  opening  the  joint  to  discover 
the  absence  of  organic  disease.  The  result  of  such  operations, 
fortunately,  if  aseptic,  is  that  the  patient  usually  recovers 
from  her  pains. 


CHAPTER   XIX 

EEFLEXES 

For   clinical   purposes    we   have   to    consider   three   varieties    of 
reflexes  : — 

(1)  Superficial  or  skin  reflexes,  e.g.  the  plantar  reflex. 

(2)  Deep  or  tendon  reflexes,  e.g.  the  knee-jerk. 

(3)  Organic    or    visceral    reflexes,    e.g.    vomiting,    micturition, 

parturition. 

Of  these  three  groups,  the  first  two  have  to  do  with  striated 
voluntary  muscles.  They  have  their  reflex  centres  within  the 
cerebro-spinal  axis,  and  many  of  them  can  be  inhibited  by  voluntary 
efiort.  The  third  group,  that  of  the  visceral  reflexes,  is  concerned 
not  with  voluntary  muscles  alone,  but  also  with  involuntary  non- 
striated  muscles  which  are  controlled  by  the  sympathetic  nervous 
system  and  are  incapable  of  direct  voluntary  restraint — e.g.  the 
muscular  walls  of  the  stomach,  bladder,  rectum,  or  uterus.  Such 
visceral  reflexes  can  be  performed,  more  or  less  perfectly,  inde- 
pendently of  the  central  nervous  system.  Normally,  visceral 
functions  go  on,  for  the  most  part,  unconsciously.  But  even 
they  may  occasionally  evoke  consciousness,  as  when  visceral  pain 
occurs,  or  when  striated  voluntary  muscles  are  required  to 
supplement  an  act  originally  initiated  by  non-striated  muscles, 
or  when  the  reflex  act  causes  stimulation  of  a  cerebro-spinal 
sensory  nerve.  Thus,  to  take  an  example,  the  act  of  defsecation 
is  practically  unconscious  and  uncontrollable,  so  far  as  the  move- 
ment of  the  large  intestine  is  concerned.  But  when  the  lower  end 
of  the  anal  canal  has  its  mucosa  stimulated,  the  perineal  muscles 
come  into  action,  and  the  act  then  becomes  a  conscious  one  and  is 
more  or  less  under  control. 

Skin  Reflexes. — These  are  movements  obtained  by  slight  stimu- 
lation of  certain  areas  of  skin  or  mucous  membrane.  The  result 
is  a  movement,  quick  or  slow,  of  the  skin  near  the  point  of  stimula- 

316 


REFLEXES 


317 


tion,  but  not  exactly  under  it.  In  certain  animals  such  as  the 
horse,  skin  reflexes  can  be  obtained  by  touching  almost  any  part 
of  the  trunk.  But  in  man  the  skin  as  a  whole  is  less  mobile,  and 
it  is  usually  only  from  certain  special  areas  that  skin  reflexes  can 
be  ehcited.  If  the  stimulus  be  too  strong,  it  may  cause  a  reflex 
so  violent  as  to  involve  almost  all  the  voluntary  m_uscles  of  the 
body.  Or  if  the  stimulus,  even  though  slight,  be  a  painful  one,  as 
for  example  a  pin-prick,  the  result  is  a  rapid  "  defensive  "  move- 
ment— e.g.  sudden  flexion  of  a  Hmb  or  abrupt  closure  of  the  eye. 

The  following  table  gives  a  hst  of  the  chief  skin  reflexes  which 
are  of  clinical  importance,  and  the  mode  of  testing  each.  All 
are  more  easily  elicited  in  young  people  than  in  old ;  in  fact, 
if  we  wish  to  demonstrate  the  skin  reflexes  with  certainty,  we 
select  a  child  for  our  subject. 


Method  of  Eliciting. 

Result. 

Segmental 
Level. 

Ciinjunctival    .     . 

Toucliing  cornea. 

Orbicularis  oculi  contracts. 

riiai-yimeal .    .     . 

Touching  posterior  wall  of  pharynx. 

Pharynx  contracts. 

Palatal     .... 

Touching  soft  palate. 

Palate  is  elevated. 

Scapular.     .     .     . 

Strokingskin  in  inter-scapul;irregion. 

Scapular  muscles  contract. 

C.5  to  Till. 

Epigastric   .     .     . 

Stroking  downwards  froui  nipple. 

Epigastrium    dimples    on    side    of 
stimulus. 

Th7  to  Th9. 

Abtlominal  ,     .     . 

Stroking     downward     from     costal 

Abdominal  muscles  contract  on  side 

Thll  to  LI. 

margin. 

of  stimulus. 

Creniasteiic     .     . 

Stroking  inner  and  upper    part  of 
thigh.    Or  pressm-e  over  Hunter's 
canal,  or  over  adductor  tubercle. 

Testicle  is  pulled  up. 

LI  and  L2. 

0 luteal    .... 

Stroking  skin  of  buttock. 

Gluteal  muscles  contract. 

L4  and  L.^. 

Pjuutar   .... 

Stroking  sole  of  foot. 

Tensor    fasciae    femoris     contracts, 
hallux  and  other  toes  flex,  ankle  is 
dorsi-flexed. 

Lo  to  S2. 

l'>iilV)o-Cavernosus 

Pinching  dorsum  of  glans  penis 

Bulbous  urethra  contracts. 

S3  and  S4. 

Superficial  Anal  . 

Pricking  skin  of  perineum. 

External  anal  sphincter  contracts. 

S5  and 

-- 

Coccygeal. 

Absence  of  the  abdominal  reflex  is  not  uncommon  in  acute 
abdominal  conditions,  notably  in  appendicitis  and  enteric  fever.'^  In 
young  adults  whose  abdominal  walls  are  apparently  normal  and 
in  whom  there  is  no  oedema  or  excessive  obesity,  absence  of  this 
reflex  is  strongly  suggestive  of  disseminated  sclerosis,  as  has  been 
pointed  out  by  Striimpell,  E.  MuUer,^  and  others.  Exaggeration  of 
the  abdominal  reflexes  is  fairly  common  in  the  gastric  or  intes- 
tinal crises  of  tabes,  being  associated  with  cutaneous  hyper- 
sesthesia  of  the  abdomen. 


1  RoUeston,  Brain,  1906,  p.  99. 

-  Neurologisches  Gentralhlatt,  1905,  p.  593. 


318 


NERVOUS   DISEASES 


Of  all  the  superficial  reflexes,  the  flantar  reflex  is  the  one 
which  has  the  greatest  practical  importance.  In  order  to  test  it, 
the  patient  should  be  lying  down,  his  feet  being  comfortably 
warm.  The  limb  to  be  tested  is  now  partially  flexed  at  the  hip  and 
knee,  and  also  rotated  so  as  to  rest  on  its  outer  side.  Then  with 
some  hard  object  such  as  the  end  of  a  penholder,  we  gently  stroke 
the  sole  of  the  foot  from  behind  forwards,  especially  towards  its 
inner  side.  Meanwhile  we  watch  carefully  for  the  fijst  movement 
of  the  great  toe.  Normally  this  is  a  movement  of  plantar  flexion 
(see  Fig.  174).  The  movement  of  the  other  toes  is  of  less  im- 
portance. It  is  interesting  also  to  note  that,  simultaneously  with 
the  toe  movement  (a  "  cortical  "  reflex)  we  have  a  brisk  con- 
traction of  the  ten- 
sor fasciae  femoris 
(Brissaud's  reflex), 
medullary  in  origin, 
which  may  occur 
even  in  cases 
where  the  toes 
show  no  move- 
ment. This  proves 
that  the  plantar  reflex  is  not  a  phenomenon  confined  to  the  foot 
but  that  it  implicates  the  whole  lower  limb.  If  we  employ  a 
stimulus  which  is  too  strong,  we  may  have,  in  addition,  dorsiflexion 
of  the  ankle,  and  this  may  obscure  the  toe  movement.  Hence 
the  importance  of  a  gentle  stimulus,  graduated  so  as  just  to 
elicit  the  toe  phenomenon  and  no  more. 

This  normal  plantar  reflex,  flexor  in  type,  only  occurs  when 
the  reflex  arc  is  intact,  and  when,  in  addition,  the  lower  reflex 
arc  is  in  connection  with  the  cerebral  motor  cortex  by  an  un- 
injured pyramidal  tract.     In  this  sense  it  is  a  "  cortical  "  reflex. 

If  the  pyramidal  tract,  conveying  motor  impulses  downwards 
from  the  cortical  "  leg-centre,"  be  interrupted  in  any  part  of  its 
course  by  injury  or  disease,  or  if  it  be  non-developed,  as  in 
infants  who  have  not  learned  to  walk,  the  type  of  plantar  reflex 
is  different  and  is  known  as  BabinsTci's  phenomenon,  or  the  extensor 
plantar   reflex,   whose    spinal    path,   traversing  the  lumbo -sacral 


Fig.  174  — Normal  plantar  reflex. 


REFLEXES 


319 


region,  is  no  longer  controlled  by  pyramidal  impulses.  In 
this  sense  it  is  a  pure  "  spinal "  reflex.  In  the  Babinski  pheno- 
menon, stimulation  of  the  sole  produces  extension  of  the  hallux 
instead  of  flexion  (see  Figs.  174  and  175).  Moreover,  this  extensor 
movement  of  the  great  toe  is  slower  than  is  the  normal,  brisk 
flexion.  Sometimes,  in  addition  to  extension  of  the  hallux,  we 
observe  a  fan-like  spreading  out  of  the  toes — "  phenomene 
d'eventail."  An  extensor  plantar  reflex  is  practically  always 
pathological,  except  in  infants  too  young  to  walk  (generally  dis- 
appearing after  the  age  of  six  months),  and  if  constantly  present 
it  indicates  an  organic  lesion,  and  one  which  implicates  the 
pyramidal  tract.  ^ 
It  is  therefore  of 
the  utmost  value 
in  the  diagnosis  be- 
tween hysteria  and 
organic  disease. 

Somewhat  re- 
sembling the  Bab- 
inski reflex,  but 
apparently  distinct 
from  it,  is  Gordon's" 
paradoxical  flexor  reflex,  which  consists  in  an  extension  movement 
of  the  great  toe  or  of  all  the  toes  when  we  press  deeply,  through  the 
calf  muscles,  between  the  heads  of  the  gastrocnemius,  on  to  the  deep 
flexor  muscles  beneath.  To  elicit  this  reflex,  the  physician  should 
place  himself  on  the  outer  side  of  the  patient's  leg,  the  muscles  of 
which  must  be  completely  relaxed.  This  is  attained  either  by  direct- 
ing the  patient  to  lie  on  his  back  or  making  him  sit  with  his  feet  on 
a  stool.  The  "  paradoxical  flexor  reflex  "  is  never  present  in  health  : 
it  occurs  only  in  organic,  and  especially  in  irritative,  lesions  of  the 
pyramidal  tract.  It  is  sometimes  associated  with  the  Babinski 
leflex,  but  may  occur  in  cases  where  the  Babinski  sign  is  absent. 

^  There  is  one  exception  to  this  rule.  This  is  in  the  case  of  a  lower 
motor  neurone  lesion  affecting  the  flexor  muscles  of  the  toes  and  sparing 
the  extensors.  In  such  a  case  the  only  possible  movement  would  be  ex- 
tension. But  the  other  signs  of  lower  neurone  lesion,  especially  the  electrical 
reactions,  will  prevent  error.  ^  American  Medicine,  1904,  p.  971. 


Fig.  175. — Babinski's  extensor  plantar  reflex. 


320  NEEVOUS    DISEASES 

Oppenheim's  reflex,  a  contraction  of  the  extensor  longus  hallucis 
and  tibialis  anticus,  is  elicited  in  a  slightly  different  way,  viz.,  by 
firm  stroking  with  some  hard  object  (such  as  the  handle  of  a 
percussion-hammer)  just  behind  the  postero-internal  border  of  the 
tibia,  from  above  downwards.  Its  significance  is  the  same  as  that 
of  the  paradoxical  flexor  reflex. 

The  cremasteric  reflex  is  very  easy  to  ehcit  in  young  children,  by 
stroking  the  inner  side  of  the  thigh.  But  in  old  men  it  is  sluggish 
or  apparently  absent.  Even  in  them,  however,  it  can  usually  be 
elicited  by  sudden  firm  pressure  backwards  against  the  sartorius 
muscle  in  the  region  of  Hunter's  canal,  or  against  the  adductor 
tubercle  of  the  femur ;  this  often  succeeds  when  stroking  the  skin 
in  the  usual  fashion  is  of  no  avail.  The  cremasteric  reflex  is  some- 
times exaggerated  on  the  affected  side  in  cases  of  sciatic  neuralgia. 

The  bulbo-cavernosus  reflex  is  of  great  diagnostic  value  in 
determining  whether  the  lowest  segments  of  the  spinal  cord  are 
intact  in  a  lesion  about  the  level  of  the  third  sacral  segment — 
where  the  ordinary  reflexes  of  the  lower  limbs  give  us  no  help. 
To  obtain  the  bulbo-cavernosus  reflex,  we  place  one  finger  behind 
the  patient's  scrotum,  pressing  upwards  against  the  bulbous  part 
of  the  urethra.  With  the  other  hand  we  pinch,  or  prick  with 
a  pin,  the  dorsum  of  the  glans  penis.;  the  bulbous  urethra  is  at 
once  felt  to  give  a  brisk  twitch.  Loss  of  this  reflex  indicates  a 
lesion  somewhere  in  its  reflex  arc,  either  in  the  anterior  cornua 
of  the  third  and  fourth  sacral  segments,  or  in  the  corresponding 
motor  or  sensory  roots  of  the  cauda  equina.  Loss  of  the  bulbo- 
cavernosus  reflex  is  a  fairly  common  sign  in  tabes,  being  due  in 
that  case  to  a  lesion  of  the  afferent  fibres  of  the  reflex  arc. 

The  superficial  anal  reflex  can  be  easily  obtained  by  pricking 
the  skin  of  the  perineum  with  a  long  "  bonnet-pin,"  and  watching 
whether  the  external  sphincter  contracts.  This  reflex  is  sometimes 
lost  in  anaesthesia  of  the  perineum,  or  in  lesions  of  the  fifth  sacral 
or  of  the  coccygeal  segment,  or  of  their  corresponding  motor  roots. 

Organic  hemiplegia  usually  produces,  at  first  at  least,  loss  of 
the  unilateral  superficial  reflexes  all  down  the  paralysed  side,  with 
one  exception — viz..  the  plantar  reflex,  which  persists,  but  from  the 
first  is  changed  into  the  extensor  type.     In  hysterical  hemiplegia, 


REFLEXES 


321 


on  the  other  hand,  even  though  cutaneous  hemi-ansesthesia  be 
present,  the  unilateral  skin  reflexes  on  the  paralysed  side  are 
usually  preserved,  with  the  exception  of  the  plantar  reflex  which 
is  often  lost.  An  extensor  plantar  reflex  never  occurs  in  pure 
hysteria.  In  hysteria  there  may  be  absence  not  only  of  any  toe 
movement  on  stimulation  of  the  sole,  but  there  may  also  be  loss  of 
the  reflex  contraction  of  the  tensor  fasciae  femoris.  This  "  com- 
bined "  absence  of  reflex  movement  both  of  the  toes  and  of  the 
fascia  lata  of  the  thigh  is  always  strongly  suggestive  of  hysteria. 
It  is  probably  due  to  a  latent  muscular  spasm. 


Fig.  176.— Method  of  eliciting  jaw-jerk. 

Deep  or  Tendon  Reflexes. — The  following  table  gives  a  list 
of  those  deep  reflexes  which  we  commonly  study  when  investi- 
gating cases  of  nervous  disease  : — 


Method  of  Eliciting. 

Eesult. 

Segmental 
Level. 

Jaw 

Tapping   lower   jaw,   supported    in 
half-open  position. 

Jaw  closes. 

Pons. 

Biceps     .... 

Tapping  biceps  tendon. 

Biceps  contracts. 

C5  and  CG. 

Supinator  longus 

Tapping  styloid  process  of  radius. 

Supinator  longus  contracts. 

05  and  C6. 

Scapulo-humeral 

Tapping  vertebral  border  of  scapula, 

Teres    minor,    Infraspinatus, 

C5  and  06. 

near  base  of  spine. 

&c.,  contract. 

Wrist 

Tapping  upper  part  of  radius. 

Wrist  and  fingers  extend. 

06  to  OS. 

Triceps    .... 

Tapping  triceps  tendon. 

Triceps  contracts. 

07  to  Thl. 

Carpo-nietacarpal 

Tapping  dorsum  of  wrist. 

Fingers  flex. 

08  and  Thl. 

Knee 

Tapping  patellar  tendon. 

Vastus  internus,  &c.,  contract. 

L3  and  L4. 

Ankle 

Tapping  tendo  Achillis. 

Calf  muscles  contract. 

Sl  and  S2. 

X 


322 


NERVOUS    DISEASES 


The  knee-jerk  may  be  taken  as  a  type  of  these  tendon  reflexes. 
It  has  been  a  matter  of  dispute  whether  it  is  really  a  true  reflex 
or  not.  Strictly  speaking,  the  jerk  occurs  too  soon  after  the  tap 
for  a  nerve  impulse  to  have  time  to  travel  up  to  the  reflex  centre 
in  the  cord  and  down  again  to  the  muscles.  But  so  long  as  the 
reflex  arc  is  intact,  there  is  a  constant  "  reflex  tonus  "  in  the  vastus 


Fig.  177. — Knee-jerk.     Reinforcement  by  Jendrassik's  method. 

internus  muscle  which,  when  the  tendon  is  struck,  permits  the 
jerk  to  occur.  If  this  reflex  tonus  be  lost  from  interruption  of 
the  reflex  arc  at  any  point,  the  jerk  can  no  longer  be  obtained. 
Therefore,  for  practical  purposes,  the  knee-jerk,  though  not  a  true 
reflex  action  itself,  is  an  index  of  the  integrity  of  the  reflex  arc. 

To  obtain  the  knee-jerk,  we  feel  for  the  patellar  tendon  and 
strike  it  either  with  the  edge  of  the  hand  or  with  some  other  fairly 
heavy  object,  such  as  a  rubber  percussion-hammer  or  a  heavy 


REFLEXES 


323 


paper-knife.  The  result  is  a  brisk  contraction  of  the  quadriceps. 
If  we  grasp  the  vastus  internus  with  our  other  hand  we  can  feel 
the  jerk  in  cases  where  it  is  too  feeble  to  move  the  knee- 
joint.  The  knee  must  be  somewhat  bent  to  put  the  quadriceps 
slightly  on  the  stretch,  and  the  muscles  must  be  absolutely  re- 
laxed.   This  latter  point  is  of  importance  ;  for  sometimes  it  happens 


Fig.  178. — Knee-jerk.     Reinforcement  by  Laufenauer's  method. 

that  a  patient  may  have  his  muscles  in  a  state  of  excessive  spasm, 
so  that  we  may  fail  to  eUcit  the  knee-jerk,  and  yet,  if  we  succeed 
in  relaxing  the  muscles  by  passive  movements,  the  knee-jerk  is 
not  only  present  but  found  to  be  increased.  The  knee-jerk  in  such 
a  case  is  not  absent,  but  only  "  concealed "  by  the  spasticity 
of  the  muscles. 

In  testing  the  knee-jerk  the  patient  may  be  sitting  on  a  table 


324  NERVOUS    DISEASES 

with  his  legs  dangling  in  the  air,  or  better,  on  a  chair  with  the 
soles  of  the  feet  flat  on  the  ground  and  the  knees  gently  semi- 
flexed, or  one  knee  may  be  crossed  over  the  other.  A  feeble  jerk 
may  be  "  reinforced  "  either  by  Jendrassik's  method  (Fig.  177), 
in  which  the  patient  hooks  both  hands  together,  pulUng  them  one 
against  the  other,  and  looks  up  towards  the  ceihng,  thereby  diverting 


Fig.  179. — Method  of  eliciting  ankle-jerk. 

his  attention  and  relaxing  the  leg  muscles.  An  even  better 
method  of  reinforcement  is  Laufenauer's,  in  which  we  grasp  the 
patient's  quadriceps  whilst  the  patient  sits  with  his  soles  flat  on 
the  ground.  The  patient  then  grasps  our  upper  arm  with  one 
hand,  and  suddenly  squeezes  when  told  to  do  so ;  meanwhile, 
down  comes  the  percussion-hammer  (Fig.  178).  The  advantage 
of  this  method  is  that  we  can  feel  for  ourselves  whether  the  patient 
really  is  directing  his  attention  to  the  act  of  reinforcement.     More- 


REFLEXES 


325 


over,  this  method  can  be  employed  to  reinforce  feeble  reflexes  of 
the  upper  limbs,  whereas  Jendrassik's  method  is  only  available 
for  reflexes  of  the  lower  limbs.  Many  other  methods  of  reinforce- 
ment have  also  been  suggested,  e.g.  by  making  the  patient  gaze 
at  the  ceiling  and  draw  a  long  breath  (Kronig-^),  or  by  making 
him  read  aloud  from  a  newspaper  or  book  as  fast  as  possible 
(Rosenbach  ^) . 


Fig.  180.— Supinator-jerk. 

Reinforcement  will  make  a  feeble  jerk  more  evident ;  but  it 
has  no  effect  if  the  jerk  be  absent. 

The  ankle-jerk  has  a  diagnostic  significance  equal  to  that  of 
the  knee-jerk.  To  test  it,  we  make  the  patient  kneel  on  a  chair 
with  his  feet  projecting  over  the  edge,  and  then  tap  the  tendo 
Achilhs  (Fig.  179) ;  a  brisk  extension  movement  of  the  ankle  is 
the  result.  In  tabes  the  ankle-jerk  is  often  lost  before  the  knee- 
jerk.  In  sciatica  loss  of  the  ankle-jeik  indicates  a  neuritis  as 
distinguished  from  a  mere  neuralgia. 

In  the  upper  extremity  we  have  various  deep  reflexes  at  our 
disposal.     Of  these,  the  supinator-jerk  is  ordinarily  the  most  acces- 

^  Berlin  klin.  Wochenschrift,  1906,  No.  44. 
^  Miinchener  med.  Wochenschrift,  1907,  No.  2. 


326  NBKVOUS   DISEASES 

sible.  In  testing  it,  we  support  the  patient's  hand  in  a  semi- 
supinated  posture,  with  the  elbow  loosely  bent  to  a  right  angle. 
We  tap  with  our  hammer  close  above  the  styloid  process  of  the 
radius  (Fig.  180).  The  supinator  longus  at  once  contracts  and 
produces  a  flexion  movement  of  the  elbow.  To  elicit  the  triceps- 
jerk,  the  best  way  is  not,  as  stated  in  some  text-books,  to  allow 
the  elbow  to  hang  over  the  back  of  a  chair,  but  rather  to 
support  the  upper  arm  horizontally,  with  the  elbow  loosely  flexed 
at  a  right  angle.  Then,  feeling  for  the  triceps  tendon,  we  tap 
it  with  our  hammer,  and  the  muscle  at  once  contracts. 

Loss  of  Deep  Reflexes. — Sometimes  these  reflexes  cannot  be 
elicited,  even  on  reinforcement.  This  is  almost  always  pathological 
(although  in  very  rare  cases  a  healthy  individual  is  found  to  be 
devoid  of  deep  reflexes),  and  generally  indicates  a  lesion  of  the  reflex 
arc.  If  this  lesion  be  in  the  afferent  limb  of  the  arc,  there  may  also 
be  anaesthesia  of  the  corresponding  nerve-  or  root-area.  If  it  be 
in  the  anterior  cornu,  or  in  the  efferent  motor  path,  there  will  be 
muscular  paralysis,  \\dth  atrophy  of  the  particular  muscle. 

The  following  is  a  list  of  some  of  the  chief  conditions  in  which 
there  is  loss  of  the  deep  reflexes  : — • 

Disease.  Site  of  Lesion. 

Neuritis  (Alcohol,  Diabetes,  Diphtheria,  Lead,  Arsenic,  ~| 

Tubercle,  Cachexia,  &c.) ]■  Peripheral  nerves,  sensory  or  motor. 

Peripheral  Nerve  Palsies j 

Tabes  Dorsalis \ 

General    Paralysis    of    Insane    (tabetic    type  —  Tabo-  | 

Friedrefch's  Ataxia       '.        '.        '.        '.        '.        '.        '.        '.  /  Posterior  columns  of  cord. 

Subacute    Combined    Degeneration    of    Posterior    and  i 

Lateral  Columns — late  stage  of J 

Any  focal  lesion  in  Grey  Matter  of  Cord     ....  Pi,eflex  centre  in  cord. 

Infantile  Paralysis  (Acute  Anterior  Poliomyelitis)    .        .  \ 

Progressive     Muscular     Atrophy     (Chronic     Anterior  I 

Poliomyelitis) \  »    ^    •  r       j 

Amyotrophic  Lateral  Sclerosis >  Anterior  cornua  of  cord. 


Syringomyelia 

Thrombosis  of  Anterior  Spinal  Artery 

Landry's  Paralysis /Anterior     cornua     and     peripheral 

•'  ■'  \     motor  nerves. 

Myopathies  (Pseudohypertrophic  and  Atrophic  types)     .    )  ht^„„„,„  if„oif 

Amyotonia  congenita j  Muscle  itseit. 

Increased    Intra-Cranial    Pressure    (especially    Hydro- 
cephalus and  Tumours  of  Posterior  Fossa). 
Pneumonia. 

Family  Periodic  Paralysis  (during  attacks). 

Immediately  after  attack  of  Major  Epilepsy  (post-epileptic  coma). 
During  Spinal  Ansesthesia. 
Complete  transverse  lesion  of  Cord. 

From  this  list  we  see  that,  in  addition  to  permanent  organic 
lesions  within  the  reflex  arc  itself,  there  are  other  conditions  where 


REFLEXES  327 

tlie  deep  reflexes  are  abolished.     Tlius  these  reflexes  are  lost  in 

the  final  stages  of  increased  intra-cranial  pressure,  especially  in 

hydrocephalus  and  in  tumours  of  the  posterior  fossa. 

This  is  attributed  by  Eaymond  and  others  to  a  curious  degeneration  of 
the  posterior  spinal  roots,  which  sometimes  occurs  in  such  conditions,  whereas 
van  Gehuchten  ^  ascribes  it  to  loss  of  function  of  the  rubro-spinal  tracts,  from 
pressure  on  the  mesencephalon. 

The  knee-jerks  are  often  lost  during  pneumonia.  In  the  attacks 
of  the  rare  disease  known  as  family  periodic  paralysis  (see  p.  253), 
the  deep  reflexes  in  the  affected  hmbs  are  temporarily  abolished, 
owing  to  temporary  paralysis  of  the  muscle-fibres.  The  deep  jerks 
are  abolished  for  a  few  minutes  just  after  an  epileptic  fit,  during 
the  stage  of  coma  and  flaccidity.  Spinal  anaesthesia  temporarily 
abolishes  all  the  deep  and  superficial  reflexes  in  the  lower  limbs 
(see  p.  419).  We  should  also  remember  that  in  coniflete 
trans-section  of  the  spinal  cord,  all  the  deep  reflexes  below  the 
level  of  the  lesion  are  lost.  If,  however,  the  lesion  be  not  com- 
plete, and  there  still  survives  some  nervous  tissue  connecting  the 
upper  and  lower  portions,  then  the  deep  reflexes  are  exaggerated. 
In  both  instances  the  plantar  reflex,  if  present,  is  extensor  in  type. 

Exaggeration  of  Deep  Reflexes. — Sometimes  the  deep  reflexes 
are  exaggerated,  so  that  the  slightest  tap  on  the  tendon  produces 
an  unusually  brisk  contraction.  This  may  be  the  result  of  various 
poisons — e.g.  tetanus,  or  strychnine-poisoning — rendering  the  reflex 
centres  unduly,  explosive  ;  or  it  may  occur  in  simple  neurasthenia. 
But  organic  lesions  of  the  pyramidal  tract  are  by  far  the  com- 
monest causes  of  permanent  exaggeration  of  the  deep  reflexes.  In 
cases  of  organic  disease,  we  look  also  for  the  presence  of  clonus. 
A  clonus  is  a  rhythmic  series  of  muscular  contractions,  produced 
by  sudden  passive  stretching  of  the  tendon,  the  clonus  continuing 
so  long  as  the  tension  of  the  tendon  is  maintained. 

Ankle-clonus  is  the  commonest  clinical  variety  of  clonus.  To 
elicit  it,  the  knee  is  passively  flexed  (the  angle  of  flexion  varying 
in  different  cases),  and  the  ankle  is  suddenly  dorsiflexed  by  upward 
pressure  on  the  sole  of  the  foot  (Fig.  181).  Ankle-clonus  is  due, 
as   Weir-Mitchell   has   pointed   out,   to    contraction,    not   of  the 

1  Le  Nevraxe,  1907,  vol.  ix.  p.  39. 


328 


NERVOUS   DISEASES 


gastrocnemius' but  of  tlie  soleus  muscle,  since  tlie  position  of  the 
knee  which  is  best  for  eliciting  ankle-clonus  is  one  in  which  the 
gastrocnemius  is  relaxed. 

A  s'purious  ankle-clonus  is  sometimes  obtained  in  cases  of  hysteria. 
This  can  usually  be  differentiated  from  genuine  clonus  by  a  char- 


FiG.  181. — Method  of  eliciting  ankle-clonus. 

acteristic  feehng  of  voluntary  contraction  in  the  muscles,  especially, 
at  the  commencement  of  the  clonus,  difficult  to  describe  in  words 
Spurious  clonus  is  generally  poorly  sustained  and  often  irregular 
in  rhythm.     It  is  never  associated  with  an  extensor  plantar  reflex. 

Knee-clonus  or  rectus-clonus  is  best  obtained  by  sudden  down- 
ward traction  on  the  patella,  the  knee  being  passively  extended. 

In  chronic  organic  affections  of  the  pyramidal  tract,  practically 
every  one  of  the  deep  jerks  may  become  exaggerated  into  clonus. 


REFLEXES  329 

Thus  in  advanced  disseminated  sclerosis  we  may  find  in  the  same 
patient  jaw-clonus,  elbow-clonus,  wrist-clonus,  finger- clonus,  knee- 
clonus,  ankle-clonus,  toe-clonus,  &c. 

The  presence  of  true  clonus  indicates  that  the  reflex  arc  is 
hyper-excitable,  owing  to  withdrawal  of  the  regulating  or  restrain- 
ing influence  normally  exerted  through  the  pyramidal  tract.  Ex- 
aggeration of  the  deep  reflexes  is  therefore  one  of  the  cardinal  signs 
of  a  chronic  lesion  of  the  upper  or  cortico-spinal  motor  neurone. 

It  is  unnecessary  to  give  a  list  of  the  various  organic  diseases 
in  which  the  deep  reflexes  are  exaggerated.  Sufiice  it  to  say  that 
any  chronic  lesion  of  the  pyramidal  tract  will  produce  exaggeration 
of  the  deep  reflexes  below  the  level  of  the  lesion.  Thus  in 
paraplegia  due  to  myehtis,  to  lateral  sclerosis,  or  to  some  other 
affection  of  the  lateral  columns,  or  in  hemiplegia  from  organic 
brain  disease,  there  is  exaggeration  of  the  deep  reflexes  in  the 
paralysed  limbs,  owing  to  injury  or  disease  of  the  pyramidal  fibres. 

There  is  an  important  exception  to  this  rule,  to  which  we 
have  already  referred,  namely  in  total  trans-section  of  the  spinal 
cord,  as  in  some  cases  of  fractured  spine.  Such  total  lesion 
produces  a  permanent  flaccid  paralysis  of  the  lower  limbs,  with 
loss  of  the  deep  reflexes.  But  if  the  lesion  be  incomplete,  we  have 
the  usual  spastic  type  of  paraplegia,  with  increased  deep  reflexes. 
In  both  instances,  whether  the  lesion  be  total  or  partial,  we  have 
an  extensor  type  of  plantar  reflex. 

We  should  also  mention  that  in  the  early  stages  of  peri'pheral 
neuritis  the  deep  reflexes  may  be  exaggerated.  But  this  soon 
passes  off  and  is  succeeded  by  their  diminution  and  loss.  Again, 
in  subacute  combined  degeneration  of  the  lateral  and  posterior 
columns  of  the  cord,  there  is  an  early  stage  of  spasticity  with 
increased  deep  reflexes,  and  a  terminal  stage  of  flaccid  paralysis 
with  loss  of  reflexes. 

Sometimes  in  spastic  paraplegia  the  muscular  rigidity  of  the 
paralysed  Hmbs  is  so  excessive  that  it  may  be  almost  impossible 
to  obtain  the  knee-jerks  and  other  deep  reflexes,  which  we  should 
ordinarily  in  these  cases  expect  to  find  exaggerated.  This  is 
because  the  muscles  are  already  in  a  state  of  tonic  spasm.     But 


330 


NEEVOUS    DISEASES 


if  we  succeed  in  temporarily  relaxing  them,  by  passive  changes 
of  posture,  we  can  sometimes  obtain  the  increased  jerks  and  even 
the  clonus.  In  most  cases,  the  spasticity  and  the  presence  of 
an  extensor  plantar  reflex  will  prevent  errors  in  diagnosis. 

Pupillary  Light  Reflex. — This  occupies  a  special  category  of  its 
own.  The  reflex  is  ehcited  by  exposing  the  pupil  to  hght,  after 
previous  shading.  Normally  under  such  conditions  the  pupil 
contracts  briskly,  both  when  stimulated  directly  and  when  the 
pupil  of  the  opposite  eye  is  exposed  to  hght  (consensual  reflex). 
In  some  respects  the  pupil  reflex  to  light,  although  occurring  in  a 
non-striated  muscle,  is  analogous  to  a  deep  reflex,  and  it  is  useful 
to  remember  that  in  tabes  this  reflex  disappears,  as  do  the  ordinary 
tendon-reflexes.  But  the  subject  of  the  various  pupil-reflexes  and 
their  connections  with  the  third  nerve,  with  the  ciHary  ganglion, 
and  with  the  cervical  sympathetic  is  discussed  elsewhere  (see 
"  Cranial  Nerves,"  p.  127,  and  "  Cervical  Sympathetic,"  p.  336). 

Organic  Motor  Reflexes. — These  are  concerned  with  the 
sympathetic  nervous  system  and  with  the  contraction  of  non- 
striated,  involuntary  muscles.  The  contraction  of  non-striated  or 
smooth  muscles  is  slow,  unhke  the  brisk  twitch  of  a  reflex  in  a 
striated  muscle.  The  following  is  a  hst  of  organic  reflexes  which  are 
of  diagnostic  interest.  In  some  of  these,  such  as  the  ciho-spinal 
or  the  scrotal,  the  reflex  movement  is  executed  entirely  by  non- 
striated  muscle.  In  others,  such  as  the  vesical,  uterine,  or  rectal, 
the  non-striated  muscle  is  reinforced  by  voluntary  striated  muscles. 


Cilio-spinal 
Scrotal    . 


Vesical 
Rectal 


Genital 
Uterine 


Method  of  Eliciting. 


Pinching'  or  scratching  skin  of  neck. 

Repeated  stroking  of  perineum  or  ap- 
plication of  cold. 

Distension  or  irritation  of  bladder  or 
posterior  urethra. 

Distension  or  irritation  of  upper  part 
of  rectum. 

From  cerebrum  or  periphery. 

Distension  or  stimulation  of  uterus. 


Internal  anal  .      Distension  of  anus  by  finger. 


Result. 


Pupil  dilates. 
Dartos  contracts. 

Bladder-wall  contracts. 

Rectum  contracts. 

Erection  of  corpora  cavernosa. 

Uterus  contracts. 

Internal  sphincter  an!  contracts. 


In  all  of  them,  with  the  exception  of  the  ciho-spinal,  the  reflex 
movement  can  be  accomphshed,  more  or  less  perfectly,  independ- 
ently of  the  central  nervous  system. 


REFLEXES  331 

In  some  text-books  the  statement  is  made  that  the  reflex 
centres  for  the  bladder,  uterus,  and  rectum  are  situated  within 
the  cord.  But  within  recent  years  cHnical  and  pathological 
evidence  has  been  brought  forward,  notably  by  L.  R.  Miiller, 
showing  that  the  lowest  reflex  centres  for  the  contraction 
of  the  bladder,  and  of  the  neighbouring  hollow  viscera 
possessing  non-striated  muscular  walls,  are  situated  extra- 
spinally,  in  the  hypogastric  and  hsemorrhoidal  plexuses  of  the 
sjnnpathetic. 

The  sympathetic  vesical  centre  can  be  stimulated  from  the 
cerebro-spinal  system.  Micturition  in  the  adult  is  a  voluntary 
act,  but  only  to  this  extent  that  it  can  be  voluntarily  initiated. 
This  is  accomphshed  by  contracting  the  diaphragm  and  abdominal 
walls,  producing  a  rise  in  the  intra-vesical  tension,  which  starts 
the  reflex ;  meanwhile  the  striated  constrictor  urethrse  is 
voluntarily  relaxed.  But  the  non-striated  bladder-wall  itself,  the 
so-called  detrusor  urinse,  is  not  under  control  of  the  will.  Once 
started,  the  bladder  empties  itself  spontaneously,  and  we  can  stop 
the  act  only  by  forcibly  innervating  the  constrictor  urethrse, 
usually  a  matter  of  considerable  effort.  But  reflex  micturition 
is  often  excited  by  irritation  of  the  urethra,  especially  of  its 
vesical  end.  Thus  if  a  few  drops  of  urine  trickle  into  the 
prostatic  urethra,  an  imperious  reflex  act  of  micturition  results, 
which  is  difiicult  to  prevent.  Similar  phenomena  are  produced  by 
the  irritation  of  a  posterior  urethritis. 

The  fibres  from  the  brain  and  spinal  cord  to  the  sympathetic 
vesical  centre  reach  it  through  the  lowest  spinal  roots,  from  the 
third  to  the  fifth  sacral,  so  that  lesions  of  the  spinal  cord  or  cauda 
equina  constantly  cause  bladder  trouble.  This  generally  takes  the- 
form  of  initial  retention  of  urine,  foUowed  after  several  days  by  in- 
termittent rejlex  incontinence  ("  incontinenza  a  getto  "  of  ItaHan 
writers  ^),  in  which  the  bladder  contracts  intermittently  and  expels 
the  urine  at  intervals.  Such  reflex  incontinence  is  generally  associ- 
ated with   incomplete    emptying,   so    that   a   certain   amount   of 

'   Deutsche  Zeitschrift  fiir  Nervenheilkunde,  1901,  Band  21,  s.  86. 
^  Rebizzi,  Rivista  di  Patologia  Nervosa  e  Mentale,  1905,  p.  80. 


332  •  NERVOUS   DISEASES 

"  residual  urine  "  remains  in  the  bladder.  In  cases  of  coma  or  of  the 
deep  insensibihty  of  fevers  such  as  typhoid,  we  observe  an  initial  re- 
tention of  urine,  followed  by  distension,  paralysis  of  the  bladder-waU 
and  overflow  dribbhng  ("  incontinenza  per  regurgito  "). 

The  sensory  nerves  from  the  bladder  pass  through  the  sym- 
pathetic by  the  rami  communicantes,  and  along  the  posterior  roots 
into  the  spinal  cord.  They  serve  to  inform  us  of  the  distension 
of  the  bladder.  There  are  also  higher  micturition  centres,  some  in 
the  spinal  cord  (in  the  lower  sacral  segments) ,  others  higher  still  in 
the  brain,  in  the  corpus  striatum  and  optic  thalamus  ;  others,  high- 
est of  all,  in  the  motor  cortex,  between  the  arm  and  leg  centres, 
controlling  the  sub-cortical  and  spinal  centres.  When  these 
higher  centres,  spinal  or  cerebral,  are  hyper- excitable,  whether 
from  disease  or  from  emotion,  we  may  have  preci'pitancy  of 
micturition,  or  even  enuresis,  a  condition  in  which  the  brain  and 
spinal  cord  on  the  slightest  provocation  send  impulses  which  relax 
the  compressor  urethrae.  A  similar  condition  exists  in  infants 
who  have  not  learned  to  control  their  subcortical  micturition 
centres. 

True  dribbling  of  urine  ("  incontinenza  vera  "),  as  distinguished 
from  intermittent  contraction  of  the  bladder,  occurs  most  typically 
in  cases  of  tabes  and  is  mainly  due  to  anaesthesia  of  the  bladder, 
which  being  now  insensitive  to  distension,  is  no  longer  stimulated 
to  contract  by  the  normal  accumulation  of  urine.  The  tabetic 
patient  with  an  anaesthetic  distended  bladder  expels  his  urine,  not 
by  contraction  of  the  bladder  but  by  pressure  with  his  abdominal 
walls.  This  can  readily  be  verified  if  we  have  to  pass  a  catheter 
for  the  purpose  of  emptying  a  tabetic  patient's  bladder.  True 
dribbhng  also  occurs  in  an  over- distended  bladder  which,  from 
obstruction  in  the  prostate  or  urethra,  has  become  flaccid,  paralysed 
and  atonic. 

The  internal  anal  reflex  is  tested  by  inserting  a  finger  within 
the  anus.  NormaUy  the  finger  is  tightly  grasped  by  the  non- 
striated  internal  sphincter.  This  reflex  is  independent  of  the 
superficial  anal  reflex  of  spinal  origin,  to  which  we  have  already 
referred.     When  the  internal  anal  reflex  is  lost,  the  anus  no  longer 


EEFLEXES  333 

grasps  the  finger  but  remains  open  for  several  seconds,  "  yawning," 
after  the  finger  has  been  withdrawn.  Such  loss  is  most  commonly 
due  to  anaesthesia  of  the  anus,  as  in  tabetic  or  other  lesions  of  the 
Cauda  equina.  The  result  is  incontinence  of  faeces.  If  there  be  a 
lesion  within  the  spinal  cord,  above  the  spinal  centre  in  the  conus 
medullaris,  there  is  intermittent  rectal  incontinence.  But  if  the 
lesion  be  in  the  afferent  nerves  from  the  rectum,  the  internal 
sphincter  remains  relaxed,  and  the  fseces,  if  fluid,  dribble  away 
continuously  when  they  enter  the  rectum,  the  patient  being 
unconscious  of  the  fact. 

To  test  the  scrotal  reflex,  which  is  an  excellent  example  of  a 
purely  sympathetic  motor  phenomenon,  the  patient  stands  bend- 
ing forwards  with  his  legs  wide  spread  and  scrotum  hanging  free. 
The  skin  of  the  perineum  is  now  stroked  with  some  hard  object 
five  or  six  times  in  succession.  After  a  few  seconds  an  extremely 
slow,  worm-hke  contraction  appears  in  the  non-striated  dartos 
muscle,  beginning  near  the  perineal  part  of  the  scrotum  and 
spreading  forwards.  This  reflex  can  also  be  elicited  by  the  applica- 
tion of  cold  to  the  perineum  or  scrotum. 


CHAPTER   XX 

AFFECTIONS   OF   THE   SYMPATHETIC.     ANGIO-NEUROSES 

To  most  of  us  the  mention  of  the  Cervical  Sympathetic  recalls 
memories  of  our  early  days  as  students  of  physiology,  and  more 
particularly  the  memory  of  a  classic  experiment  of  Claude  Bernard 
upon  the  rabbit.  But  it  is  perhaps  not  sufficiently  reahsed  that 
the  cervical  sympathetic  is  also  of  considerable  chnical  importance. 
First  of  all,  let  us  recall  a  few  anatomical  points.  The  sympa- 
thetic nervous  system  forms  two  gangliated  cords,  coursing  hke  two 
strings  of  beads,  one  on  each  side,  close  in  front  of  the  vertebral 
column,  and  extending  from  the  base  of  the  skull  to  the  front 
of  the  coccyx.  Above,  these  chains  are  connected  with  plexuses 
which  enter  the  cranial  cavity ;  below,  they  converge  and  end 
in  a  loop  on  the  coccyx.  Each  chain  is  made  up  of  multipolar 
nerve-cells  and  nerve-fibres,  all  of  them  involuntary  fibres  des- 
tined mostly  for  organs  which  possess  smooth  muscle-fibres  and 
for  blood-vessels.  In  addition  to  its  own  longitudinal  fibres,  the 
sympathetic  chain  receives  connecting-fibres  from  the  central 
nervous  system.  These  are  called  the  rami  communicantes — some 
of  them  white,  some  of  them  grey.  They  unite  the  sympathetic 
to  the  anterior  primary  divisions  of  the  spinal  nerves.  The  white 
rami,  consisting  of  meduUated  fibres,  pass  from  the  spinal  cord 
to  the  sympathetic  gangha ;  they  are  all  efferent  in  function, 
and  leave  the  cord  through  the  anterior  nerve-roots.  A  certain 
number  of  white  rami,  viz.  those  emerging  along  with  the  seventh, 
ninth,  and  tenth  cranial  nerves,  and  those  emerging  with  the 
second  and  third  sacral  nerves,  pass  directly  to  the  viscera  and 
blood-vessels,  to  end  in  small  peripheral  ganglia,  without  joining 
the  sympathetic  chain  itself.  To  these  two  sets  of  splanchnic 
nerve-fibres,  cranial  and  sacral,  the  name  'para-sym'pathetic  fibres 
has  been  given,  to  distinguish  them  from  the  ordinary  sympathetic 


AFFECTIONS  OF  THE  SYMPATHETIC  335 

nerves  and  ganglia.  The  grey  rami,  consisting  of  non-medullated 
fibres,  originate  in  the  sympathetic  ganglia,  and,  Hke  the  others, 
join  the  spinal  nerves.  Some  of  them  are  afferent,  going  into 
the  spinal  cord,  reaching  it  through  the  posterior  nerve-roots  ; 
others  turn  off  with  the  peripheral  nerves  and  supply  to  the  skin 
involuntary  efferent  fibres,  whose  functions  are  vaso-motor,  vaso- 
inhibitory,  pilo-motor,  secretory,  &c.  In  addition,  the  sympathetic 
cords  give  branches,  either  directly  or  through  the  great  pre- 
vertebral gangha  (the  cardiac,  solar,  and  hypogastric  plexuses), 
to  the  various  glands  and  viscera  of  the  body,  to  the  heart  and 
blood-vessels,  to  the  genital  organs,  and  to  the  non-striped 
muscles  of  the  body  generally. 

In  addition  to  the  ordinary  ganglia  of  the  sympathetic  chain, 
there  are  also  minute  micro- sympathetic  ganglia  or  hypospinal 
ganglia  of  Marinesco  and  Minea,^  which  are  so  small  that  they 
can  only  be  identified  by  microscopic  examination  of  the  spinal 
nerves  immediately  below  the  junction  of  the  anterior  and 
posterior  nerve-roots.  These  microscopic  ganglia  are  closely  con- 
nected with  the  rami  communicantes.  Their  precise  function  is 
still  obscure. 

Lastly,  the  cervical  part  of  the  sympathetic  chain  has  very 
special  "  oculo-pupillary  "  fibres,  which  are  cUnically  of  consider- 
able importance.  These  supply  the  dilator  pupillae,  the  non- 
striated  part  of  the  levator  palpebrae  superioris  and  the  orbital 
muscle  of  Mliller — a  small  bundle  of  non-striated  muscle  which  lies 
behind  the  globe  of  the  eye  and  bridges  across  the  spheno- 
maxillary fossa  at  the  back  of  the  orbit.  The  cervical  sympathetic 
also  supphes  secretory  fibres  to  the  submaxillary  gland,  and, 
Hke  the  sympathetic  elsewhere,  it  suppUes  fibres  to  the  cutaneous 
blood-vessels,  also  (through  the  hypoglossal  nerve)  to  the  vessels 
of  the  tongue,  and,  lastly,  fibres  to  the  sweat-glands  of  the  head 
and  neck. 

The  pupil-dilating  fibres  have  a  pecuhar  course,  which  it  is 
important  to  remember  (see  Fig.  182).  Arising  from  the  pupil- 
dilating  centre  in  the  medulla,  they  descend  in  the  lateral  column 

1  Neurologisches  Gentralblatt,  1908,  s.  146. 


336 


NERVOUS    DISEASES 


of  tlie  spinal  cord  to  the  ciKo-spinal  centre  in  the  lower  cervical 
region.  They  emerge  from  the  cord  through  the  anterior  roots  of 
the  first  and  second  thoracic  segments,  and  enter  the  inferior 
cervical  ganglion  of  the  cervical  sympathetic  by  white  rami 
communicantes.     They  then  ascend  in  the  cervical  sympathetic  to 


To  noTV'Striccted/  paurt  of/ 
Jdey.PaZp.Sup. 


MEDVLLA\ 


TTpperLvob. 


CiHo-spinaL  Centre- 


Long  CilLccry  Nerves. 
Gobsserixav  Ganglion. 

^Mubscle  of  MiUler 
(jwrv-striateci). 

ToMyp  oglossaJbNervR. 

H  ,,^^^—SweoLbJPihres. 
^  y^^'-^YobSo-rrwtcr  & 
^y^^  yaso-dHator Fibres. 

Middle  CervicaL  GounglLorv. 


p  Inferior  Cervical  GangKon,. 


Fig.  182. — Diagram  of  course  of  oculo-pupillary  fibres  of  cervical 
sympathetic. 

the  Gasserian  ganglion  and  pass  thence  to  the  orbit  (along  the 
ophthalmic  division  of  the  fifth  cranial  nerve),  and  vid  the  long 
cihary  nerves  to  the  pupil.  They  do  not  traverse  the  ciliary 
ganglion  (see  Fig.  55,  p.  127). 

It  is  evident  that  ocular  and  other  symptoms  may  be  produced 
not  only  by  lesions  of  the  ascending  fibres  of  the  cervical  sympa- 
thetic, but  also  by  lesions  within  the  cord,  affecting  the  fibres  in 


AFFECTIONS    OF    THE    SYMPATHETIC  337 

their  downward  course  from  the  medulla  (this  being  remarkably 
frequent  in  syringobulbia  and  in  unilateral  lesions  of  the  medulla), 
or  by  lesions  of  the  first  two  thoracic  nerves  or  of  their  anterior 
roots,  or  even  by  lesions  of  the  ophthalmic  division  of  the  fifth 
cranial  nerve,  though  this  last  is  rare. 

The  signs  of  paralysis  of  the  cervical  sympathetic  are  very  char- 
acteristic. Fig.  183  shows  a  woman  who  was  sent  to  hospital  with 
the  history  that  six  years  previously  she  had  some  tuberculous 
glands  removed  from  the  right  side  of  her  neck.  When  she 
recovered  from  the  ansesthetic,  she  learned  that  the  jugular  vein 
had  been  injured  during  the  operation.  But  other  structures  had 
also  been  injured,  and  amongst  them  was  the  cervical  sympathetic 
(which  lies  behind  the  carotid  sheath),  because  afterwards  she 
noticed  that  the  right  eyelid  drooped  a  little,  that  the  right 
side  of  the  face  flushed  less  than  the  left,  and  that  when  she 
chewed,  a  small  patch  of  excessive  perspiration  appeared  below 
the  right  eye.  We  observe  from  the  photograph  that  the  right 
pupil  is  smaller  than  the  left,  from  paralysis  of  the  dilator 
pupillae.  Moreover,  the  affected  pupil  does  not  dilate  when 
shaded,  yet  it  contracts  briskly  to  hght  and  on  convergence, 
since  the  third  cranial  nerve,  which  through  the  ciliary  ganghon 
innervates  the  sphincter  pupillse,  is  unaffected.  Further,  we 
notice  that  the  upper  lid  droops,  making  the  palpebral  fissure 
narrower  than  on  the  healthy  side.  This  is  due  to  paralysis  of 
the  non-striated  part  (tarsalis  superior)  of  the  levator  palpebrae, 
which  is  inserted  into  the  upper  edge  of  the  tarsal  cartilage.  The 
voluntary,  striated  fibres  of  the  levator,  inserted  into  the  skin  of  the 
upper  lid  and  supplied  by  the  oculo- motor  nerve,  are  unaffected, 
and  the  patient  is  therefore  able  to  elevate  the  lid  voluntarily 
to  its  full  extent.  This,  therefore,  is  not  a  true  ptosis,  but  a 
"  pseudo-ptosis." 

We  also  notice  that  the  right  eye  has  sunk  into  the  orbit,  owing 
to  paralysis  of  the  non-striated  orbitalis  muscle  of  Miiller,  which 
normally  keeps  the  globe  pressed  forwards.  This  "  enophthalmos  " 
narrows  the  palpebral  fissure  still  more.  The  difference  in  antero- 
posterior projection  between  the  two  eyes  is  seen  best  if  we  make 


338 


NERVOUS   DISEASES 


the  patient  lie  down,  we  then  stand  behind  and  look  down  at 
the  forehead  and  eyeballs  from  above. 

On  palpating  the  two  globes,  we  find  that  the  intra-ocular 
tension  is  diminished  on  the  affected  side. 

Such  are  the  "  oculo-pupillary  "  symptoms  of  cervical  sympa- 
thetic paralysis.  There  are,  however,  one  or  two  additional  points. 
When  the  cervical  sympathetic  is  paralysed,  it  no  longer  responds 
to  stimulation.     There  are  two  clinical  ways  of  stimulating  it.     One 


Fig.  183. — Paralysis  of  cervical  sympathetic  on  the  right  side.  The 
black  line  encloses  an  area  of  ansesfchesia,  due  to  division  of 
cutaneous  nerves. 

is  by  pinching  or  pricking  the  side  of  the  neck,  when  we  produce  a 
dilatation  of  the  pupil  on  the  same  side  ;  this  "  cilio-spinal  reflex  " 
is  abohshed  in  cervical  sympathetic  palsy.  Another  method  of 
stimulating  the  cervical  sympathetic  is  to  drop  into  the  conjunctiva 
a  few  minims  of  a  solution  of  cocaine.  The  result  is  that  the 
pupil  dilates,  the  upper  lid  retracts,  and  the  eyeball  is  pushed 
shghtly  forwards.  All  these  phenomena  were  absent  in  the 
patient  just  referred  to.  She  also  told  us  that  when  her  face  flushes, 
it  does  so  only  on  the  healthy  side.     Moreover,  her  face  on  the 


AFFECTIONS    OF    THE    SYMPATHETIC  339 

affected  side  no  longer  sweats  except  in  one  little  patch,  below  the 
orbit,  where  it  sometimes  sweats  spontaneously  when  sh.e  chews. 
To  verify  this  point  we  made  her  sweat  profusely  by  means  of 
pilocarpin,  and  found  that  the  right  side  of  the  face  remained  dry, 
except  in  a  small  area  below  the  inner  canthus  of  the  eye.  This 
survival  of  a  little  oasis  of  sweating  on  the  dry  side  might  perhaps 
mean  that  a  small  twig  of  the  sympathetic  had  escaped  injury. 


Fig.  181. — Paralysis  of  the  left  cervical  sympathetic  from  a  tumour 
at  the  root  of  the  neck. 

or  more  probably  that  sweat  fibres  to  that  part  of  the  face  are 
supplied  through  a  branch  of  the  trigeminal  nerve. 

So  much  for  lesions  of  the  sympathetic  chain  itself.  But  the 
oculo-pupillary  and  other  fibres  may  also  be  damaged  at  some 
point  between  the  spinal  cord  and  the  inferior  cervical  ganglion. 
Fig.  184  represents  a  boy  of  seventeen  who  had  felt  a  tinghng  sensa- 
tion down  his  left  arm  for  several  months.  A  few  weeks  before 
he  came  under  observation,  he  noticed  that  a  swelHng  had 
appeared  in  the  lower  part  of  the  neck  on  the  same  side.  At  a 
glance  we  see  that  the  cervical  sympathetic  is  affected.  There 
are  pseudo-ptosis,  myosis,  and  enophthalmos.       The   left    cheek 


340 


NERVOUS   DISEASES 


is  a  little  fuller  than  the  right.  The  cilio-spinal  reflex  was 
absent  on  the  left  side.  On  examining  the  root  of  the  neck, 
we  found  that  the  left  clavicle  was  bulged  forwards  at  its  inner 
end,  the  supra-clavicular  fossa  being  filled  up.  Further,  there 
was  percussion- dulness  all  over  the  apex  of  the  left  lung,  with 
diminution  of  breath  sounds  and  of  vocal  resonance.  There  was 
also  a  strip  of  diminished  sensation  to  touch  and  pain  along  the 
inner  side  of  the  left  upper  hmb,  reaching  to  the  wrist  and  corre- 
sponding to  the  cutaneous  areas  of  the  first  and  second  thoracic  roots. 
Moreover,  there  was  shght  wasting  of  the  hypothenar  muscles  of 


Fig.  185. — Radiogram,  showing  tumour  at  apex  of  left  lung, 
in  patient  represented  in  Fig.  184. 


the  left  hand,  supplied  by  the  first  thoracic  root.  The  skin  of 
the  left  hand  was  dry,  whilst  that  of  the  right  was  moist,  and  the 
patient  himself  noticed  that  in  hot  weather  only  the  right  side  of 
his  face  sweated.  On  comparing  corresponding  arteries  of  both  sides 
we  found  that  the  pulse  in  the  left  upper  limb  was  smaller  than  in 
the  right.  All  this  pointed  to  the  presence  of  a  sohd  mass  behind 
the  left  clavicle,  compressing  the  subclavian  artery,  aflecting  the 
first  and  second  thoracic  nerves,  including  not  only  their  sensory  and 
motor  fibres  but  also  the  cervical  sympathetic  fibres.  This  diagnosis 
was  confirmed  by  radiography,  which  showed  very  clearly  (Fig.  185) 
a  tumour  at  the  apex  of  the  left  lung.     This  tumour  grew  rapidly 


AFFECTIONS    OF    THE    SYMPATHETIC  341 

compressed  the   subclavian   vein,   producing   oedema   of  the   left 
upper  limb,  and  within  six  months  the  patient  died. 

Fig,  186  is  that  of  a  seaman  on  an  Atlantic  liner  who  was 
thrown  by  a  heavy  sea  against  an  iron  rail,  rupturing  the  whole 
of  the  brachial  plexus  on  the  right  side.  He  was  unconscious 
for  a  number  of  days,  and  during  this  period  he  was  trephined 
over  the  left  Rolandic  area  on  the  supposition  that  the  paralysis 


Fig.  186. — Rupture  of  brachial  plexus  on  right  side.     Total  ansesthesia 
of  right  upper  limb  below  black  line. 


of  the  arm  was  of  cerebral  origin.  In  addition  to  complete  motor 
and  sensory  paralysis  of  the  upper  Hmb,  obviously  of  lower  motor 
neurone  type,  resulting  from  the  brachial  plexus  palsy,  he  showed 
very  beautifully  the  oculo-pupillary  signs  of  cervical  sympathetic 
paralysis  on  the  right  side — enophthalmos,  myosis  and  pseudo- 
ptosis (see  Fig.  187).  In  this  patient,  however,  the  pupil  still 
dilated  to   cocaine,  probably  because   some   pupil-dilating   fibres, 


342 


NERVOUS    DISEASES 


entering  the  cervical  sympathetic  from  the  second  thoracic  root, 
had  escaped  injury. 

Figs.  188  and  189  are  those  of  a  soldier  who  came  under  my 
observation  dm^ing  the  South  African  war  in  1901.  He  had  been 
wounded  in  the  neck  by  a  Mauser  bullet.  At  the  time  of  his 
injury  he  was  lying  on  his  face,  firing  at  the  enemy.  The  bullet 
entered  his  neck  an  inch  and  a  half  below  the  left  mastoid  process, 
crossed  the  middle  line  in  front  of  the  vertebral  column,  and  came 
out  through  the  seventh  right  interspace  in  the  posterior  axillary 


Fig.  187. — raralysis  of  right  cervical  sympathetic  from  rupture  of 
brachial  plexus. 


line,  lodging  in  his  bandolier.  He  immediately  felt  a  sensation 
"  hke  an  electric  shock  "  all  over  his  body,  but  especially  in  the 
right  upper  extremity,  which  became  at  once  totally  paralysed. 
He  had  haemoptysis  owing  to  the  perforation  of  the  lung,  and 
for  a  few  days  some  difficulty  of  swallowing,  probably  due  to  injury 
of  the  oesophagus.  In  about  three  weeks  the  haemoptysis  gradually 
ceased,  and  the  right  upper  hmb  recovered  power,  so  that  when 
I  first  saw  him,  two  and  a  half  months  after  the  injury,  he  was 
able  to  move  it  freely  at  all  joints.     Ever  after  the  accident  he 


AFFECTIONS    OF    THE    SYMPATHETIC 


343 


noticed  that  he  did  not  sweat  on  the  right  side  of  the  face  and 
neck,  nor  in  the  right  upper  Hmb. 

The  photographs  show  that  the  patient  has  an  area  of  slight 
analgesia  (bounded  by  the  thick  black  line)  along  the  inner  border 
of  the  right  upper  hmb,  corresponding  to  the  areas  supphed  by 
the  eighth  cervical,  first  thoracic,  and  second  thoracic  nerve-roots. 
He  also  has  slight  weakness  of  the  small  muscles  of  the  thumb, 


Fig.  188. 


Fig.  189. 


Figs.  188  and  189. — Paralysis  of  the  right  cervical  sympathetic,  from  a 
bullet  wound  of  the  lower  roots  of  the  brachial  plexus.  The  area 
of  the  right  upper  limb  within  the  black  line  is  ansesthetic.  The 
crosses  on  the  trunk  indicate  the  boundary  of  an  area  of  anidrosis. 

innervated  by  the  first  thoracic  root.  We  also  observe  that  the 
right  cervical  sympathetic  is  paralysed,  so  that  he  has  contraction 
of  the  pupil,  enophthalmos,  and  pseudo-ptosis  on  that  side. 

But  there  is  a  point  of  special  interest  in  this  patient's  photo- 
graphs. They  demonstrate  a  point  which,  so  far  as  I  know,  had 
not  previously  been  mapped  out  in  the  human  subject,  viz.,  the 
extent  of  skin  supphed  with  sweat-fibres  by  the  cervical  sympa- 
thetic.      In  the  tropical  heat  to  which  we  were  exposed,  this 


344 


NERVOUS    DISEASES 


patient  sweated  profusely,  except  in  an  area  on  the  right  side 
of  the  head,  neck,  upper  Hmb,  and  upper  part  of  the  trunk.  That 
area  remained  dry,  and  the  boundary  between  sweating  and  non- 
sweating  skin  was  sharp  and  distinct.  In  order  to  photograph 
it,  the  happy  thought  occurred  to  blow  powdered  charcoal  on 
the  skin.  This  stuck  on  the  sweating  side,  and  blew  off  on  the  dry 
side.     We  were  then  able  to  photograph  the  non-sweating  area,  to 

which  the  cervical  sympa- 
thetic should  have  been 
distributed.  As  may  be  seen 
from  the  photographs  (Figs. 
183  to  190),  the  boundary  of 
this  area,  marked  by  crosses, 
runs  down  the  middle  Hne 
of  the  head  and  neck,  and 
turns  horizontally  across  the 
chest  at  the  level  of  the 
third  rib  in  front  and  the 
spine  of  the  scapula  behind, 
including  the  whole  of  the 
upper  limb. 

Before  leaving  the  subject 
of  cervical  sympathetic  palsy, 
it  should  be  mentioned  that 
excision  of  the  cervical  sym- 
pathetic has  been  employed 
therapeutically  in  certain 
diseases.  Thus  in  cases  of  glaucoma,  ophthalmic  surgeons  have 
recommended  this  operation  to  diminish  the  intra-ocular  tension, 
and  a  certain  amount  of  benefit  has  resulted.  Bilateral  excision 
of  the  cervical  sympathetic  has  also  been  tried  for  the  rehef  of 
epilepsy,  in  the  hope  of  paralysing  the  cerebral  vasomotor  nerves 
and  thereby  rendering  the  brain  hyperaemic,  especially  in  cases 
where  fits  were  ushered  in  by  blanching  of  the  face.  But  the 
results  recorded  have  not  been  sufficiently  good  to  warrant  us  in 
recommending  this  procedure. 


Fig.  190. — Paralysis  of  the  right  cervical 
sympathetic,   showing  oculo-pupillary 
phenomena  and  area  of  anidrosis. 


APFECTIONS    OF    THE    SYMPATHETIC 


345 


Let  us  now  consider  briefly  the  reverse  condition,  viz.,  irrita- 
tion or  stimulation  of  the  cervical  sympathetic.  The  signs  are 
exactly  the  opposite  of  those  produced  by  paralysis.  We  there- 
fore have  dilatation  of  the  pupil,  exophthalmos  or  forward  projection 
of  the  eyeball,  widening  of  the  palpebral  aperture  (Stellwag's  sign), 
and  delayed  descent  of  the  upper  lid  when  the  patient  looks 
downwards  (von  Graefe's  sign).  All  these  phenomena  can  be  pro- 
duced, to  a  certain  degree,  by 
dropping  into  a  healthy  eye 
a  solution  of  cocaine,  which 
stimulates  the  cervical  sym- 
pathetic. 

Fig.  191  is  that  of  a  man 
who  had  lymphadenomatous 
enlargement  of  the  lymphatic 
glands.  During  his  stay  in 
hospital,  we  noticed  that  quite 
rapidly,  within  a  day  or  two, 
he  developed  on  the  right 
side  exophthalmos,  widening 
of  the  palpebral  fissure,  and 
some  dilatation  of  the  pupil. 
There  was  also  in  hospital  at 
the  same  time  a  soldier  who 
had  similar  signs  in  one  eye 
due  to  an    aneurism  at  the 


Fig.  191. — Stimulation  of  the  right  cer- 
vical sympatlietic. 


root  of  the  neck,  pressing  on  and  irritating  the  cervical  sym- 
pathetic. If  such  pressure  continues,  the  signs  of  stimulation 
may  pass  ofi  and  be  replaced  by  those  of  paralysis.  Our  lympha- 
denomatous patient,  however,  died  nine  weeks  after  the  ap- 
pearance of  stimulation  phenomena,  without  any  change  in  the 
direction  of  paralysis. 

Certain  cases  of  apical  phthisis  and  apical  pneumonia 
are  accompanied  by  inequahty  of  the  pupils,  probably  due 
to  irritation  of  the  cervical  sympathetic  by  changes  in  the 
pleura.      There    is    a    good   deal    in    favour   of    the    view   that 


346  NERVOUS    DISEASES 

many  of  the  signs  of  exophthalmic  goitre  are  the  result  of 
stimulation  of  the  sympathetic,  whether  by  excessive  or  per- 
verted thyroid  secretion.  Figs.  192  and  193  are  from  a  case'  of 
exophthalmic  goitre  where  the  symptoms  were  preponderatingly 
right-sided.  The  tachycardia  of  this  disease  is  probably  due  to 
stimulation    of    cardio-accelerator    fibres,    which    we    know     are 


Fig.  192.  Fig.  193. 

Exophthalmic  goitre,  the  ocular  symptoms  being  more  marked  on  the  right 
side.  Fig.  193  shows  von  Graefe's  sign  in  the  right  eye  on  looking 
downwards. 

derived  from  the  sympathetic.  The  thyroid  enlargement  may 
perhaps  be  explained  as  a  result  of  vasomotor  paralysis  of  the 
cervical  vessels,  including  those  of  the  thyroid  gland  itself.  The 
leucopenia  of  polymorph  cells  in  the  blood,  together  with  the 
excess  of  lymphocytes,  is  probably  a  secondary  result  of  the 
disordered  thyroid  secretion. 

But  though  affections  of  the  cervical  sympathetic  are  the  most 
readily  recognised,  we  must  not  forget  that  the  thoracic  and 
abdominal   portions    of  the   sympathetic    may   also    be    diseased, 


ANGIO-NEUROSES  347 

although  the  symptoms  thereby  produced,  being  mainly  visceral, 
are  less  easy  of  diagnosis.  Thus  some  cases  of  angina  pectoris 
may  be  the  result  of  irritation  of  the  cardiac  plexus,  while  the 
peculiar  rejflex  vaso-constriction  of  the  pulmonary  vessels,  with  its 
transient  dilatation  and  irregularity  of  the  right  heart,  met  with 
in  certain  gastric  and  hepatic  disorders,  has  been  regarded  as 
an  affection  of  the  thoracic  part  of  the  sympathetic.  Affections 
of  the  abdominal  sympathetic  or  of  its  great  pre-vertebral  ganglia 
produce  still  more  striking  clinical  phenomena.  Thus  the  rare 
condition  known  as  acute  dilatation  of  the  stomach,  and  many  of 
the  symptoms  of  acute  peritonitis,  such  as  the  intestinal  paralysis, 
meteorism,  small  pulse,  and  general  collapse,  may  be  the  result  of 
acute  paralysis  of  the  solar  plexus — the  "  abdominal  brain  "  ;  while 
irritation  of  the  solar  plexus  is  exemplified  in  cases  of  lead  colic, 
with  its  pain,  constipation,  and  increased  arterial  tension.  The 
various  visceral  "  crises  "  of  tabes — gastric,  intestinal,  renal,  &c. — 
may  also  be  due  to  irritative  changes  in  the  various  parts  of  the 
abdominal  sympathetic.  To  the  same  cause  also  may  be  attributed 
the  intestinal  symptoms  of  exophthalmic  goitre,  consisting  not  in 
ordinary  diarrhoea  with  loose  motions,  but  rather  in  an  abnormal 
frequency  of  defsecation.  Muco-membranous  colitis,  with  its  charac- 
teristic paroxysms,  has  been  ascribed  by  Mathieu  and  others  to 
some  disorder  of  the  solar  plexus,  though  pathological  evidence  on 
the  point  is  scanty.  To  solar  or  splanchnic  disease  may  also, 
perhaps,  be  attributed  such  affections  as  orthostatic  albuminuria, 
diabetes  insipidus,  and  certain  forms  of  glycosuria. 

In  addition  to  visceral  disorders,  disease  of  the  abdominal  sympa- 
thetic is  also  associated  with  certain  pigmentary  changes  in  the  skin. 
Of  these,  the  most  striking  examples  are  furnished  by  the  cutaneous 
pigmentation  which  is  occasionally  present  in  exophthalmic  goitre 
and,  still  more,  by  Addison's  disease,  with  its  characteristic  bronzing 
of  the  skin,  its  asthenia  and  its  paroxysmal  diarrhoea.  Addison's 
disease  is  probably  the  result  of  two  factors — ^irritation  of  the  ab- 
dominal sympathetic  and  inadequacy  of  suprarenal  function,  the 
proportional  role  played  by  each  of  these  varpng  in  different  cases. 

Angio-Neuroses. — These  comprise  a  group  of  diseases  which 


348  NEEVOUS    DISEASES 

appear  to  depend  on  disorders  of  the  sympathetic  fibres  wliich 
regulate  the  blood-vessels.  A  considerable  amount  of  evidence  ^ 
points  to  the  conclusion  that  the  paroxysmal  unconsciousness  of 
epilepsy  is  associated  with  sudden  cerebral  anaemia  and  that  the 
tonic  stage  of  a  major  epileptic  fit  is  accompanied  by  cortical  anaemia, 
whilst  the  clonic  stage  is  associated  with  return  of  arterial  circu- 
lation. It  is  uncertain  what  proportion  of  these  phenomena  is 
due  to  sudden  "stoppage  of  the  heart  (we  may  sometimes  feel  the 
patient's  pulse  stop  at  the  onset  of  a  fit)  and  how  much  to  vaso- 
motor spasm  of  cortical  vessels. 

The  paroxysmal  dyspnoea  of  asthma,  with  its  slow  and 
laboured  breathing,  is  doubtless  to  be  referred  to  a  neurosis 
of  the  thoracic  sympathetic,  whether,  as  some  hold,  the 
phenomena  be  the  immediate  result  of  a  sudden  vascular  en- 
gorgement of  the  bronchial  mucous  membrane,  or  whether  produced, 
according  to  another  view,  by  spasm  of  the  non-striated  bronchial 
muscles.  In  any  case,  the  paroxysmal  nature  of  the  affection,  its 
apparent  toxic  origin  in  some  cases,  its  connection  in  other  cases 
with  nasal  or  other  reflex  sources  of  irritation,  its  frequent  asso- 
ciation with  the  gouty  diathesis — all  these  facts  indicate  a 
functional  and  not  an  organic  lesion  of  the  sympathetic. 

Most  angio-neuroses,  however,  affect  the  blood-vessels  of 
the  more  superficial  parts  of  the  body,  such  as  those  of  the 
skin  or  of  the  muscles.  Amongst  the  cutaneous  angio-neuroses, 
perhaps  the  commonest  is  the  syndrome  known  as  Raynaud's 
disease.  The  mildest  degree  of  this  is  local  rpallor  ("  local  syncope" 
or  "  dead  finger  "),  where  the  affected  parts,  usually  the  fingers, 
less  frequently  the  toes,  the  edges  of  the  ears,  or  the  tip  of  the 
nose,  suddenly  become  cold  to  the  touch  and  of  a  waxy 
white  colour.  Together  with  this,  the  patient  feels  a  tinghng 
or  other  peculiar  sensation  (acro-parsesthesia).  Actual  blunting  of 
sensation  to  touch  may  be  present.  One  or  both  hands  may  be 
affected,  sometimes  identical  fingers  in  both  hands ;  the  thumb 
is  less  often  affected  than  the  other  digits.  The  attacks  last  from 
a  few  minutes  to  several  hours  and  are  commonest  in  winter. 
1  A.  E.  Russell,  Lancet,  1909,  April  3,  10,  and  17. 


ANGIO-NEUEOSES  349 

They  are  often  brought  on  by  washing  the  hands  in  cold  water,  or 
by  fine  digital  movements  such  as  sewing  or  piano-playing.  As  the 
attack  passes  off,  the  patient  feels  a  sensation  of  tingling  or  even 
of  pain.  A  more  severe  variety  is  that  of  local  asphyxia  or  cyanosis, 
in  which  the  affected  digits  suddenly  become  discoloured,  varying  in 
tint  from  a  dusky  blue  or  slate-colour  to  an  intense  purplish- 
black.  Pressure  on  the  discoloured  area  causes  a  white  mark  which 
persists  for  several  seconds,  before  the  lividity  slowly  reappears. 
The  pain  is  usually  more  intense  than  in  local  syncope.  As 
the  attack  passes  off,  the  affected  part  often  sweats  freely.  But 
the  most  severe  variety  of  Raynaud's  disease  is  symmetrical 
gangrene,  which  is  usually  preceded  by  local  asphyxia  and  some- 
times by  local  syncope.  As  a  rule,  the  gangrenous  process  is 
confined  to  a  small  part  of  the  cyanosed  area.  In  its  mildest  form 
the  necrosis  is  limited  to  the  epithehum,  so  that  only  desquamation 
results ;  more  often  a  small  bhster  forms,  with  blood-stained 
contents.  This  bursts,  leaving  an  ulcer  which  subsequently 
cicatrises.  The  nails  may  be  lost  and  subsequently  reproduced. 
Or  the  necrosis  may  extend  deep  into  the  tissues,  forming  a  dark 
slough.  Whole  phalanges  may  undergo  dry  mummification  and 
be  cast  off,  leaving  a  conical  stump.  The  bones  as  a  rule  escape 
necrosis.  Pain  is  usually  severe  during  the  initial  cyanosis.  The 
symptoms  of  Raynaud's  disease  are  due  to  local  spasm  of  the 
vessels,  the  sudden  onset  and  disappearance  of  the  symptoms 
being  incompatible  with  any  other  hypothesis.  The  coexistent 
sensory  symptoms  are  probably  due  to  imperfect  blood-supply.  A 
paroxysm  of  local  sjmcope  or  cyanosis  can  usually  be  relieved, 
as  Gushing  has  pointed  out,  by  applying  a  tight  flat  rubber 
tourniquet  around  the  hmb  above,  so  as  to  occlude  all  the  vessels, 
both  arteries  and  veins,  and  leaving  it  on  for  several  minutes. 
Then,  when  the  tourniquet  is  taken  off,  there  is  a  temporary  vaso- 
motor paralysis,  the  whole  hmb  flushes  to  the  finger-tips,  and  a 
wave  of  redness  wipes  out  the  local  pallor  or  cyanosis.  Raynaud's 
disease  is  sometimes  associated  with  paroxysmal  hsemoglobinuria, 
probably  due  to  vasomotor  spasm  of  the  renal  vessels.  In  rare 
cases  paroxysmal  impairment  of  vision  has  been  noted,  and  during 


350  NERVOUS    DISEASES 

such  attacks  the  retinal  arteries  on  ophthalmoscopic  examination 
have  been  seen  to  be  spasmodically  contracted. 

In  striking  contrast  with  Raynaud's  disease  is  the  condition 
known  as  eryihromelalgia  (see  Plate  II.),  which  usually  attacks  one 
or  other  foot.  There  is  pain  of  a  burning  or  stabbing  character, 
often  of  excruciating  severity,  occurring  in  paroxysms  lasting 
from  a  few  minutes  to  several  hours.  This  pain  is  always  aggra- 
vated by  a  dependent  posture  of  the  limb,  by  voluntary  movement, 
or  by  warmth,  whereas  it  is  diminished  by  a  horizontal  or  elevated 
posture,  by  rest,  and  by  cold  applications.  The  earhest  attacks 
consist  simply  of  pain.  As  the  disease  progresses,  however,  redness 
and  swelling  of  the  foot  are  superadded ;  more  rarely,  redness 
precedes  pain.  The  redness  is  of  a  bright  tint,  often  confined, 
for  instance,  to  the  ball  of  the  big  toe  or  to  small  areas  of  the  sole 
or  edge  of  the  foot.  Sometimes  it  is  diffused  over  the  foot.  The 
redness  increases  in  intensity,  and  if  the  limb  be  allowed  to  hang 
down,  the  "  vascular  storm "  continues,  with  bounding  arteries, 
local  rise  of  temperature,  and  intense  cutaneous  hypersesthesia. 
As  the  attack  subsides  the  redness  is  replaced  by  cyanosis.  In  one 
case  which  I  observed,  desquamation  of  the  affected  area  occurred 
after  each  paroxysm. 

But  there  are  other  cases  in  which  the  vasomotor  symptoms 
are  intermediate  in  type  between  the  two  extremes  of  Raynaud's 
disease  and  erythromelalgia.  These  two  diseases  may  coexist,  or 
may  succeed  each  other  in  the  same  patient.  Erythromelalgia  is 
sometimes  one  of  the  earliest  signs  of  organic  cord  disease,  such 
as  disseminated  sclerosis,  and  this  points  to  its  origin  from  an 
affection  of  the  spinal  vasomotor  centres,  perhaps  in  the  "inter- 
medio-lateral "  group  of  nerve-cells  between  the  anterior  and  pos- 
terior horns,  to  which  Bruce  ^  directed  special  attention.  A  few 
rare  cases  have  also  been  observed  of  family  gangrene,  somewhat 
resembhng  Raynaud's  disease.  Fig.  194  represents  three  brothers, 
aged  five,  four  and  three  years  respectively,  in  all  of  whom,  one 
winter,  areas  of  local  necrosis  appeared  in  the  feet.  The  eldest 
child  had  necrosis  of  the  skin  of  both  heels,  followed  by  similar 

^   Trans.  Roy.  Soc.  of  Edin.,  1906,  vol.  xlv.  part  i.  p.  105. 


PLATE   II. 

Case  of  Erythromelalgia  in  a  man  aged  52.  The  condition  affected 
both  lower  limbs. 

The  upper  drawing  shows  the  appearance  of  one  foot  during  a 
paroxysm  when  the  lower  limb  is  supported  in  a  horizontal  position. 
The  sole  of  the  foot  is  of  a  bright  pink  colour,  this  colour  also  extending 
on  to  the  dorsum  of  the  terminal  phalanx  of  each  toe. 

The  lower  drawing  shows  the  effect  of  allowing  one  foot  to  hang 
dependent  for  a  few  minutes.  There  is  extreme  cyanosis  extending  as 
high  as  the  ankle.  There  was  also  severe  pain,  partially  relieved  by 
reassuming  the  horizontal  posture  of  the  limb. 


To  face  page  350. 


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ANGIO-NEUROSES 


351 


areas  on  the  dorsum  of  the  right  foot  and  on  the  fourth  left  toe. 
The  second  child  had  cyanosis  and  some  necrosis  of  the  dorsal 
surfaces  of  both  feet,  whilst  the  youngest  had  severe  necrosis  of 
the  hallux,  fourth  and  fifth  toes  on  the  right  side,  and  a  smaller 
area  of  necrosis  on  the  plantar  surface  of  the  left  hallux.  It 
is    possible    that    the    paroxysms    of    family    feriodic    ^paralysis 


Fig.  194. — Family  gangrene  in  three  brothers,  affecting  the  feet. 


(see  p.  253)  may  be  the  result  of  a  recurring  vaso-motor 
spasm  of  the  anterior  spinal  artery,  which,  as  we  have  seen, 
supphes  the  anterior  cornua  of  the  spinal  cord. 

Another  paroxysmal  disease  of  angio-neurotic  origin  is  inter- 
mittent limp,  whose  symptoms  we  have  already  described  (p.  251), 
where  the  arteries  not  of  the  skin  but  of  the  deep  structures  are 
in  a  state  of  temporary  spasm. 


352  NERVOUS    DISEASES 

Acute  angio-neurotic  cedema,  or  Quincke's  disease,  is  undoubtedly 
a  vaso-neurosis.  It  is  characterised  by  paroxysmal  attacks  of 
sbarply-localised,  bard  oedema  in  the  cellular  tissue  of  various  parts 
of  the  face,  trunk,  or  limbs.  After  lasting  a  few  hours  or  days,  the 
swelling,  which  is  remarkably  firm  and  does  not  pit  on  pressure, 
passes  off  spontaneously.  It  may  also  attack  mucous  mem- 
branes, for  example,  those  of  the  respiratory  or  gastro-intestinal 
tract.  A  gastric  attack  may  cause  urgent  vomiting,  an  intes- 
tinal attack  meteorism,  cohc,  and  bloody  diarrhoea,  and  if  the 
patient  happens  to  have  an  attack  in  the  larynx,  death  may 
result  from  asphyxia.  In  the  skin,  the  parts  most  often  attacked 
are  the  Ups,  cheeks  and  eyehds.  The  disease  sometimes  runs  in 
families. 

In  chronic  hemiplegia  it  is  not  uncommon  to  find  oedema  of  the 
hand  or  foot  on  the  paralysed  side.  Permanent  coldness  and 
cyanosis  are  very  common  in  the  paralysed  Hmbs  in  cases  of 
old  anterior  poliomyelitis.  Even  in  warm  weather  the  flaccid 
limb  remains  cold  and  sometimes  blue  in  the  hand  or  foot,  as  the 
case  may  be.  Such  cyanosis  differs  from  that  of  Rajmaud's  group 
in- being  permanent  and  not  paroxysmal. 

Certain  varieties  of  urticaria  may  be  referable  to  affection  of 
the  nervous  system,  as  in  certain  cases  where  the  characteristic 
itching  wheals  appear  on  sudden  emotional  excitement.  These 
patients  appear  to  have  a  specially  low  coagulabiHty  of  the 
blood  due  to  deficiency  of  calcium  salts  in  the  liquor  sanguinis. 
But  urticaria  is  much  more  often  toxic  in  origin.  Dermogra'phism, 
on  the  other  hand  ("  factitious  urticaria  "  or  "  urticaria  scripta  "), 
is  a  reflex  cutaneous  phenomenon.  It  is  ehcited  by  stroking 
the  skin  firmly  with  a  smooth,  hard  object,  such  as  the  head  of 
a  pin  or  the  finger-nail.  If,  for  example,  we  draw  a  diagram 
or  write  on  the  patient's  skin  in  this  way,  a  red  area  appears 
within  a  few  seconds.  The  sldn  then  becomes  elevated  into 
a  hard,  white  ridge,  which  can  not  only  be  felt  but  seen,  as  if  the 
pattern  or  writing  had  been  embossed  on  the  skin  (see  Fig.  211, 
p.  387).  This  lasts  for  many  minutes  and  passes  off  gradually 
Unlike  true  urticaria,  dermographism  is  unaccompanied  by  itching. 


ANGIO-NEUEOSES 


353 


The  phenomenon  is  commonest  in  neuropathic  people,  but  is  not 
confined  to  them  ;  it  is  particularly  common  in  exophthalmic 
goitre,^  and  may  sometimes  be  found  in  apparently  healthy 
individuals. 

Lastly,  we  have  to  refer  to  certain  abnormalities  of  sweating 
which  are  due  to  nervous  disorders.  We  have  already  alluded  to 
locahsed  anidrosis  or  absence  of  sweat  in  certain  cases  of  cervical 
sympathetic  palsy.  But  sometimes  we  meet  with  'paroxysmal 
localised  hyperidrosis  or  excessive  sweating.  Eigs.  195  and  196 
show  the  areas  of  excessive  sweating  in  two  patients.     In  one  the 


Fig.  195. — Area  of  localised 
sweating  during  masti-- 
cation  of  pungent  sub- 
stances. From  a  man 
aged  29.  The  condition 
was  congenital. 


Fig.  196. — Area  of  localised 
sweating  during  mastica- 
tion of  pungent  substances. 
From  a  man  aged  35,  in 
whom  the  condition  ap- 
peared at  the  age  of  28. 


condition  was  congenital,  and  consisted  in  excessive  sweating  on 
the  left  side  of  the  scalp  and  face,  corresponding  to  the  whole  of 
the  first  division  and  part  of  the  second  division  of  the  trigeminal. 
In  the  other,  the  whole  area  of  the  trigeminal  on  the  right  side  was 
affected  and  the  condition  appeared  at  the  age  of  twenty-eight. 
In  both  these  patients,  who  were  otherwise  healthy,  the  paroxysms 
of  sweating  occurred  only  on  chewing  highly-flavoured  articles, 
such  as  onions  or  pickles.  This  condition  suggests  some  hyper- 
excitability  of  the  {reflex  sweating  centre  for  the;  face,  possibly 
within  the  pons.  Fig.  197  is  a  photograph  of  an  area  of  hyperi- 
drosis on  the  left  hand  and  wrist  of  a  young  woman  of  nineteen. 


Dreschfeld,  Brit.  Med.  Journal,  November  18,  1905. 


354 


NERVOUS    DISEASES 


In  her,  the  paroxysms  occurred  three  or  four  times  a  day,  spon- 
taneously, chiefly  about  the  time  of  the  menstrual  period  or 
when  she  was  excited.  In  this  case  the  distribution  suggested  a 
segmental  or  root  area,  apparently  about  the  eighth  cervical  and 
first  thoracic  segments,  and  counter-irritation  over  the  lower  part 


Fig.  197. — Localised  hyperidrosis  along  ulnar  border  of  forearm  and  hand. 
The  dark  area  is  due  to  powdered  charcoal  adherent  to  sweating  skin. 


of    the   neck,    front    and    back,    near    the    exit    of  these   roots 
produced  rapid  ameHoration  of  the  condition. 

In  certain  chronic  cases  of  hemiplegia,  we  not  infrequently 
observe  excessive  sweating  of  the  hand  and  foot  on  the  paralysed 
side.  This  is  doubtless  due  to  changes  in  the  sweating  centres  in 
the  central  nervous  system. 


CHAPTER   XXI 

THE   NEUROSES 

The  boundary  between  organic  diseases  and  the  so-called  func- 
tional diseases  or  neuroses  is  entirely  imaginary.  The  old  defini- 
tion of  a  neurosis  as  a  nervous  disease  devoid  of  anatomical 
changes  is  inadequate.  Disease  is  inconceivable  without  some 
underlying  physical  basis.  The  lesion  need  not  be  visible  micro- 
scopically ;  it  may  be  molecular  or  bio-chemical.  In  certain 
diseases,  such  as  epilepsy  and  paralysis  agitans,  the  essential 
underlying  lesion  is  still  undiscovered,  yet  we  no  longer  class 
them  as  neuroses  in  the  strict  sense  of  the  word.  Therefore  when 
we  as  physicians  talk  of  neuroses,  although  we  may  have  a  fair 
general,  idea  of  what  we  mean,  we  find  it  difficult  to  express  our 
definition  in  words. 

In  "  functional "  nervous  diseases  the  underlying  physical 
changes  are  slight  in  degree  and  they  are  often  capable  of  cure. 
In  this  respect  they  differ  not  only  from  ordinary  organic  diseases 
due  to  gross  anatomical  lesions,  which  almost  always  leave  behind 
them  some  permanent  damage,  but  also  from  such  steadily  pro- 
gressive and  incurable  affections  as  paralysis  agitans.  Neverthe- 
less we  must  recognise  that  the  neuroses  are  real  diseases,  as  real 
as  smallpox  or  cancer.  A  sharp  distinction  must  be  drawn 
between  a  hysterical  or  a  neurasthenic  patient  and  a  person  who 
is  deliberately  shamming  or  malingering.  The  imitation  of  other 
diseases — neuromimesis — which  is  often  seen  in  hysteria  is  not  a 
voluntary  affair.  The  hysterical  or  neurasthenic  patient  usually 
has  no  knpwledge  of  the  disease  which  he  or  she  may  unconsciously 
simulate.  The  various  paralyses  and  pains  from  which  hysterics 
and  neurasthenics  suffer  are  as  real  to  the  patients  as  if  they  were 
due  to  gross  organic  disease. 

The  three  chief  neuroses  proper  are  neurasthenia,  psychasthenia, 

355 


356  NERVOUS    DISEASES 

and  hysteria.  Neurasthenia  is  an  "  exogenous "  neurosis ; 
psychasthenia  is  essentially  "  endogenous  "  ;  so  also  is  hysteria, 
although  outside  factors  may  act  as  exciting  or  precipitating 
causes.  Each  of  these  neuroses  has  fairly  distinctive  character- 
istics of  its  own,  but  in  practice  they  are  often  combined  with 
each  other  and  may  also  coexist  with  organic  diseases.  Thus  a 
hysterical  patient  may  sufier  from  neurasthenia,  or  a  psychasthenic 
patient  from  hysteria  ;  nor  is  there  anything  to  prevent  a  neuras- 
thenic patient  from  having,  say,  an  attack  of  cerebral  haemorrhage. 
Moreover,  any  gross  organic  disease  may  induce  hysterical  or  neur- 
asthenic phenomena  in  addition  to  the  signs  of  organic  lesion. 
In  fact  certain  cases  of  grave  organic  disease  (especially  disseminated 
sclerosis  and  some  cerebral  tumours)  may  at  first  produce  symptoms 
which  are  indistinguishable  from  those  of  functional  disease — 
which,  in  fact,  are  functional.  In  such  cases  the  neurologist  must 
be  on  his  guard  to  detect  the  underlying  organic  affection,  and  to 
distinguish  its  symptoms  from  those  of  the  superadded  hysteria 
or  neurasthenia.  Functional  symptoms,  then,  may  coexist  with 
gross  organic  disease. 

Let  us  briefly  recall  some  of  the  characteristic  symptoms  of 
the  chief  neuroses — neurasthenia,  psychasthenia,  and  hysteria — and 
note  in  what  respects  they  differ,  if  at  all,  from  analogous  symptoms 
produced  by  gross  organic  diseases. 

Neurasthenia  is  not  a  primary  disease.  It  is  exogenous,  the 
result  of  something  else.  The  commonest  cause  is  over-strain, 
mental  or  physical.  It  may  also  be  produced  by  excess  in  drugs 
such  as  alcohol,  tobacco,  or  cocaine  ;  or,  again,  by  the  toxins  of 
various  infective  diseases  such  as  influenza,  enteric  fever,  &c. 
Or  neurasthenia  may  result  from  organic  diseases,  whether  these 
be  of  the  nervous  system  {e.g.  tabes,  disseminated  sclerosis)  or  of 
other  systems  (as  in  gout,  rheumatism,  cancer,  and  so  on).  Lastly, 
a  particularly  frequent  cause  is  traumatism,  especially  in  railway 
accidents  which  produce  a  common  type  of  neurasthenia  including 
the  so-called  "  railway  spine."  Patients  with  a  low  power  of 
resistance  are,  of  course,  specially  liable  to  become  neurasthenic 
from  any  accidental  cause,   but  we   must  remember  that  even 


THE    NEUROSES  357 

healthy  individuals,  without  neuropathic  taint,  may  be  rendered 
neurasthenic  as  a  result  of  over-strain  or  trauma. 

The  symptoms  of  neurasthenia  are  chiefly  subjective.  The 
patient  complains  of  undue  fatigue  and  feebleness  of  attention, 
so  that  sustained  mental  effort  becomes  impossible — so-called 
"  brain  fag."  There  is  "  irritable  feebleness,"  with  general  depres- 
sion of  the  whole  nervous  system.  The  patient's  memory,  however, 
is  unimpaired,  and  he  relates  his  woes  with  great  wealth  of  detail. 
He  is  full  of  aches  and  pains,  but  on  physical  examination  there 
is  little  or  nothing  to  be  made  out  in  the  way  of  ansesthesia  or 
motor  paralysis.  Amongst  the  motor  symptoms,  the  chief  is 
asthenia  or  excessive  tendency  to  fatigue.  When  this  affects  the 
internal  ocular  muscles  it  constitutes  asthenopia  or  tiredness  of  the 
eyes  on  attempting  to  accommodate  as  in  reading.  Or  the  neur- 
asthenic patient  may  feel  his  limbs  tremulous  whenever  he  attempts 
any  exertion.  But  there  is  never  a  true  motor  paralysis.  Indi- 
vidual movements,  although  they  may  be  feeble  and  tremulous,  are 
never  impossible.  The  sensory  symptoms  of  neurasthenia  mclude 
subjective  sensations  ad  infiyiitum,  all  of  them  disagreeable.  Pains 
and  dyssesthesise  of  various  sorts  are  specially  common  in  the  head 
and  along  the  vertebral  column.  Vaso-motor  symptoms  are 
common,  including  a  curious  violent  pulsation  of  the  abdominal 
aorta  which  may  feel  almost  subcutaneous.  The  patient  often  com- 
plains of  sudden  flushes  of  heat  or  cold  traversing  the  trunk,  limbs, 
or  face,  also  of  paroxysmal  sweating,  and  so  on.  Sometimes  we 
can  see  transient  blotches  of  redness  at  the  sides  of  the  neck,  spread- 
ing upwards  over  the  angles  of  the  mandibles  on  to  the  cheeks. 
Gastro-intestinal  atony  is  common,  with  anorexia,  dyspepsia,  and 
constipation.  An  element  of  auto-intoxication  may  thus  be 
superadded  which  aggravates  the  general  malnutrition.  The 
superficial  reflexes  may  be  exaggerated,  especially  the  abdominal 
reflexes.  Sometimes  if  we  stroke  the  abdomen  in  a  circular  direc- 
tion the  umbihcus  moves  so  smartly  that  it  seems  to  be  chasing  our 
finger  round.  The  knee-jerks  in  neurasthenia  are  sometimes 
abnormally  brisk  and  accompanied  by  a  sudden  feehng  of  shock  in 
the  spme,  making  the  patient  start.     True  ankle-clonus,  however, 


358  NERVOUS    DISEASES 

does  not  occur,  and  the  plantar  reflexes,  if  present,  are  of  the  normal 
flexor  type.  The  sphincters  are  unaffected.  Most  neurasthenics 
are  poorly  nourished,  but  not  all  of  them.  For  purposes  of  treatment 
neurasthenic  patients  can  be  divided  into  two  classes,  viz.,  those 
in  whom  the  arterial  tension  is  above  normal,  and  those  in  whom 
it  is  abnormally  low.  The  cases  where  there  is  increased  arterial 
tension,  according  to  Fleury,  are  generally  toxic  in  origin  and  require 
special  attention  to  the  organs  of  excretion.  In  cases  with  sub- 
normal arterial  tension,  on  the  other  hand,  we  devote  ourselves 
to  augmenting  the  patient's  nervous  energy  by  anabolic  treatment 
in  the  form  of  diet,  massage,  electrical  and  hydro-therapeutic 
measures. 

Psychasthenia  is  a  much  more  serious  affection,  in  which  the 
mental  phenomena  overshadow  the  physical.  Unlike  neurasthenia, 
which  is  usually  a  disease  of  adult  life  resulting  from  some  extraneous 
cause,  psychasthenia  is  an  endogenous  disease,  the  culmination 
of  an  ingrained  neuropathic  heredity,  and  its  earliest  indications 
appear  in  adolescence  or  even  in  childhood.  In  short,  the  psych- 
asthenic, like  the  poet,  is  born,  not  made.  Moreover,  while  neur- 
asthenia is  an  eminently  curable  affection,  the  psychasthenic  patient 
remains  psychasthenic  all  his  life,  though  his  symptoms  may  be 
alleviated. 

The  outstanding  symptoms  of  psychasthenia,  as  Janet  has 
emphasised,  are  the  psychasthenic  "  stigmata,"  the  obsessions, 
and  the  imperious  acts.  The  stigmata  of  psychasthenia  may 
be  psychical  or  physical.  The  psychical  stigmata  of  psych- 
asthenia are  mental  anergia  and  irresolution.  The  psychasthenic 
feels  himself  incapable  of  fixing  his  attention,  whether  for  physical 
or  mental  effort ;  he  has  a  feeling  of  general  hesitation  and  doubt, 
and  has  to  lean  for  moral  support  on  others  possessing  a  stronger 
character  than  his  own.  This  anergia  or  defective  will-power  in 
psychasthenia  differs  from  the  anergia  of  true  melancholia  in  that 
the  psychasthenic  is  distressed  by  his  anergia,  and  whilst  desirous 
to  act,  finds  himself  unable  to  do  so,  despite  extraordinary  and 
even  agonising  efforts.  The  melancholic  patient,  on  the  other  hand, 
is  not  merely  anergic  but  also  apathetic,  and  his  failure  to  act  causes 


THE    NEUROSES  359 

him  little  or  no  distress.  Sometimes  the  psychasthenic  has  a  feeling 
of  double  personality,  in  which  he  feels  as  if  he  had  two  co-existing 
egos.  The  double  personality  of  psychasthenia  differs  from  that 
of  hysteria,  in  which  the  duality  is  an  alternating  one,  as  a  rule 
unknown  to  the  patient. 

The  physical  stigmata  of  psychasthenia  are  evidenced  in  the 
patient's  actions.  Everything  he  does  tends  to  be  clumsy  and 
gauche ;  his  very  gait  may  be  ungainly  ;  he  is  often  a  "  tiqueur  "  ; 
he  is  full  of  affectations  and  mannerisms.  In  addition  he  may  have 
numerous  neurasthenic  symptoms,  amongst  which  all  sorts  of 
cephalic  sensations  are  specially  common,  e.g.  sensations  of  fulness 
or  emptiness  in  the  head,  of  looseness  or  tightness,  of  creaking 
or  sawing,  and  so  on.  Physical  or  mental  over-exertion  or  excite- 
ment may  even  induce  an  epileptiform  fit.  Gastro -intestinal 
atony  is  common,  with  all  its  train  of  symptoms  in  the  form 
of  dyspepsia,  constipation,  &c.  ;  the  circulatory  and  vaso-motor 
systems  may  be  affected,  e.g.  by  paroxysms  of  palpitation,  attacks 
of  blushing  or  pallor,  excessive  sweating  or  abnormal  dryness  of 
the  skin  ;  the  sexual  functions  are  usually  diminished,  in  male 
patients  spermatorrhoea  is  particularly  common,  and,  as  in  neur- 
asthenia, the  general  nutrition  is  usually  below  par. 

The  second  great  characteristic  of  psychasthenia  is  the  presence 
of  obsessions  or  dominant  ideas  of  various  sorts.  These  are 
almost  always  of  a  depressing  type  and  may  be  of  the  most  varied 
forms.  A  psychasthenic  obsession  comes  on  spontaneously  in 
paroxysms  and  cannot  be  inhibited  by  any  effort  of  the  patient. 
When  the  obsession  arrives,  it  occupies  the  patient's  entire  atten- 
tion, so  that,  for  the  time,  he  can  think  of  nothing  else.  In  the  in- 
tervals between  his  paroxysms  the  psychasthenic  is  a  fairly  normal 
person,  taking  an  interest  in  the  ordinary  incidents  and  pleasures 
of  hfe.  In  this  respect  he  differs  essentially  from  the  melancholic, 
whose  depression  is  continuous,  who  lives  in  constant  gloom  and 
derives  no  pleasure  from  life.  Although  the  obsession  is  often 
an  idea  which  is  repulsive  to  the  patient,  yet  it  is  most  insistent 
and  tends  to  recur  again  and  again.  The  patient  recognises  it  as 
being  a  morbid  idea,  yet  he  cannot  throw  it  off.     The  different 


360  NERVOUS    DISEASES 

obsessions  vary  in  their  tendency  to  become  translated  into  actions. 
Thus,  though  psychasthenics  often  have  obsessions  of  suicide,  they 
very  rarely  attempt  suicide  ;  on  the  other  hand  obsessions  to  steal 
(kleptomania),  to  drink  (dipsomania),  and  to  perform  sexual  acts 
are  more  difficult  to  resist.  A  certain  proportion  of  professional 
"  tramps  "  are  simply  psychasthenic  individuals  obsessed  by  the 
impulse  to  wander  from  place  to  place,  unable  to  settle  down,  even 
when  offered  the  work  for  which  they  profess  themselves  to  be 
looking.  We  should  note  that  though  the  psychasthenic  patient 
may  have  obsessions,  he  has  no  delusions  or  hallucinations  ; 
reasoning  powers  are  unimpaired.  He  must  therefore  be  clearly 
distinguished  from  the  insane  patient. 

The  third  characteristic  feature  of  psychasthenia  is  the  occur- 
rence of  imjperious  acts  {i.e.  an  irresistible  tendency  to  perform 
some  special  act),  and  of  paroxysmal  imperious  ideas.  Imperious 
acts  include  the  innumerable  varieties  of  tics.  As  to  the  paroxysmal 
imperious  ideas,  these  include  such  varieties  as  the  mania  for  per- 
petually asking  questions  {folie  de  po7irquoi),  the  mania  of  fussy 
tidiness,  the  mania  of  counting  things  over  and  over  {aritIwioma7iia), 
the  mania  of  searching  for  objects,  and  so  on.  Manias  of  this  sort, 
of  course,  interfere  with  normal  mental  processes,  interrupting  them 
to  such  an  extent  that  the  patient  finishes  by  accomplishing  prac- 
tically nothing  in  the  way  of  mental  work.  Imperious  ideas  may 
also  be  of  an  emotional  nature  ;  these  include  the  innumerable 
forms  of  pJiohia,  such  as  agoraphobia  (fear  of  being  in  open  spaces), 
claustrophobia  (fear  of  being  inside  buildings,  especially  public 
buildings),  aichmophoba  (fear  of  sharp  objects),  rupophobia  (fear 
of  dirt),  toxicophobia  (fear  of  being  poisoned),  ereuthophobia 
(fear  of  blushing),  fear  of  death,  fear  of  illness,  fear  of  performing 
organic  functions  such  as  micturition  or  defeecation  {coprophohia), 
unreasonable  fear  of  certain  animals  or  insects,  and  so  on,  ad 
infinitum.  In  most  of  these  psychasthenic  phobias  there  is, 
coexistent  with  the  repulsion  for  the  particular  act  or  object,  a 
strong  attraction  to  that  same  object  or  act.  This  mixture  of 
apprehension  and  attraction,  as  Raymond  ^  has   pointed   out,  is 

1  Bulletin  Medicale,  1907,  No.  30. 


THE    NEUROSES  361 

one  of  the  causes  of  the  mental  agitation   which  accompanies  a 
psychasthenic  phobia. 

Lastly,  we  come  to  the  subject  of  Hysteria.  This  is  a  disease 
which  is  much  commoner  in  women  than  in  men.  It  is  more 
frequent  during  adolescence  and  adult  Hfe  than  in  childhood  or 
old  age,  although  it  may  sometimes  occur  in  little  children  of  8,  6, 
or  even  4  years.  Whilst  no  race  and  no  people  is  exempt  from 
hysteria,  it  is  relatively  more  frequent  in  the  Latin  races  and 
amongst  the  Jews.  Many  cases  of  hysteria  have  a  nervous  heredity. 
Hysterical,  alcoholic,  or  tuberculous  parents  are  prone  to  have 
hysterical  children.  We  sometimes  find  physical  or  emotional 
shocks  as  exciting  causes,  or  a  combination  of  the  two,  as  for  example 
after  an  earthquake,  a  stroke  of  hghtning,  or  a  railway  accident. 
Imitation  of  other  hysterics  may  produce  epidemics  of  hysteria, 
whether  in  adolescents  as  in  girls'  schools,  or  in  adults  as  in  certain 
religious  "  revival  meetings."  In  some  cases  disease  or  irritation  of 
the  genital  organs  is  a  causal  factor,  but  probably  much  less  fre- 
quently than  Freud  and  his  followers  would  have  us  believe. 

Hysterical  states  shade  imperceptibly  into  normal  mental 
states,  there  being  no  hard  and  fast  line  of  demarcation.  A 
certain  susceptibility  to  suggestion  and  a  certain  emotional  re- 
action exist,  of  course,  in  normal  individuals  in  widely  varying 
degrees.  Such  phenomena  are  especially  marked  in  children.  In 
fact,  as  Schnyder  ^  has  said,  we  may  speak  of  the  "  physiological 
hysteria  "  of  childhood.  But  if  an  adult  reverts  to  the  childish 
susceptibility  to  suggestion  and  to  infantile  emotional  reactions, 
we  consider  him  or  her  pathological,  hysterical  in  fact. 

For  purposes  of  convenience  we  shall  consider  the  symptoms 
in  four  groups — psychical,  sensory,  motor,  and  lastly,  visceral  and 
vascular.  In  each  of  these  groups  we  may  find  excess,  diminution, 
or  perversion  of  the  normal  nervous  processes. 

Psychical  Symptoms. — These  are  invariably  present  in  hysteria 
to  a  greater  or  less  degree.  The  most  outstanding  feature  is 
deficiency  of  inhihition.  The  patient  reacts  too  readily  to  stimuli  or 
suggestions,  whether  originating  in  the  outside  world  or  within  her 

^  Journal  de  Neurologic,  1907,  p.  281. 


362 


NERVOUS    DISEASES 


own  body.  One  of  the  most  striking  instances  of  this  is  found  in 
the  phenomena  of  hypnotic  suggestion,  whereby  a  pecuKar  form 
of  temporary  hysteria — the  hypnotic  trance — is  artificially  induced 
by  suggestion,  and  can  be  made  suddenly  to  disappear  by  the  same 
means.  This  disappearance  of  symptoms  during  or  after  hypnosis 
is  sometimes  taken  advantage  of  in  the  treatment  of  hysteria  by 
hypnotic  suggestion.  But  it  is  open  to  the  objection  that  instead 
of  strengthening  the  patient's  feeble  inhibition,   it  utilises  that 


Fig.  198. 


Fig.  199. 


Figs.  198  and  199. — Case  of  hysterical  paraplegia  of  fourteen  years' 
duration.  Showing  a  characteristic  hysterical  posture  of  the  feet 
when  the  patient  is  passively  supported. 


fault.  Yet  if  the  result  be  that  the  patient  has  a  hysterical  sup- 
pression of  her  hysterical  symptoms  (on  the  mathematical  prin- 
ciple that  —  X  —  =  +)  it  is,  to  some  extent,  a  benefit.  But 
results  obtained  by  this  plan  are  less  hkely  to  be  permanent  than 
when  we  strengthen  the  patient's  inhibition  or  self-control  by 
positive  measures. 

Deficient  inhibition  being  the  keynote  of  the  hysterical  "  '^f'l^X'?," 
we  find,  accordingly,  that  the  patient  is  excessively  emotional 
and    changeable     in    disposition,    often    excitable    and    perhaps 


THE    NEUROSES 


363 


passionate.  She  giggles  or  cries  on  slight  provocation,  and  one  of 
the  most  familiar  forms  of  hysterical  "  fit  "  consists  merely  in 
alternate  loud  laughter  and  crying.  Her  will-power  is  feeble,  she 
is  swayed  by  passing  whims  ; 
and  this  want  of  self- 
reliance  leads  to  another 
very  characteristic  sj^mptom 
— the  craving  for  sympathy. 
If  that  sympathy  be  shown, 
as  is  so  often  the  case,  to 
an  injudicious  extent  by 
the  patient's  relatives  and 
friends,  her  recovery  may 
be  indefinitely  delayed. 
Hence  it  is  generally  of 
supreme  importance  to  re- 
move the  hysterical  patient 
completely  from  her  old 
surroundings,  and  to  isolate 
her  until  the  vicious  circle 
is  broken. 

Figs.  198  and  199  are 
photographs  of  a  woman 
aged  37,  who  for  over  four- 
teen years  had  lain  on  a  bed 
of  sickness  unable  to  move 
her  legs,  a  case  of  hysterical 
paraplegia.  But  she  was 
cherished  by  the  sympathy 
of  a  devoted  mother  and  of 
various  benevolent  lady- 
visitors,  anxious  to  soothe 
her  dying  moments.  She  was  admitted  to  hospital,  and  as  a 
result  of  six  weeks  of  isolation  and  massage,  she  recovered  the 
power  of  walking,  as  will  be  seen  from  the  other  photograph 
(Fig.    200).      This   successful  result  was   due  quite  as  much   to 


Fig.  200. — The  same  patient  as  in  Figs. 
198  and  199,  after  six  weeks'  treat- 
ment, showing  restoration  of  power 
of  walking. 


364  NERVOUS    DISEASES 

the  isolation  as  to  the  other  measures,  such  as  special  diet,  and 
massage. 

It  is  convenient  to  mention  here,  in  connection  with  the 
psychical  symptoms,  the  hysterical  affections  of  speech.  Some- 
times there  is  excessive  volubihty  —  a  diarrhoea  verhorum.  In 
other  cases  we  find  the  reverse  condition  of  hysterical  mutism, 
where  the  patient  is  absolutely  dumb.  Hysterical  aphasia  usually 
deviates  in  some  gross  or  paradoxical  fashion  from  organic  aphasia. 
It  is  often  accompanied  by  curious  tricks  of  pronunciation  or  of 
intonation.  In  less  severe  cases  it  is  not  uncommon  to  find  merely 
loss  of  voice,  or  hysterical  aphonia — where  the  patient  can  only 
utter  her  tale  of  woe  in  a  whisper,  breathing  it  softly  into  the  ear 
of  a  sympathetic  listener.  Hysterical  aphonia  has  characteristic 
laryngoscopic  appearances,  in  the  form  of  adductor  paralysis  of  the 
cords,  with  which  we  are  familiar. 

Patients  with  mutism  or  aphonia  sometimes  suddenly  recover 
their  voice  when  the  dominant  obsession  is  loosened,  e.g.  by 
administration  of  chloroform  (by  the  physician),  or  of  an  excess 
of  alcohol  (by  the  patient),  or  by  some  sudden  shock,  physical 
or  mental.  Intra-laryngeal  faradism  cures  immediately  many 
cases  of  hysterical  aphonia. 

Articulation  in  hysterical  and  psychasthenic  patients  may  be 
affected  in  all  sorts  of  curious  fashions.  I  have  seen  several 
patients  who  drew  a  breath  between  each  separate  syllable, 
e.g.  "  hos — pi — ^tal."  Some  psychasthenic  "  tiqueurs  "  interpolate 
curious  barking,  grunting,  or  snorting  noises  amongst  their 
words.  One  lady  was  afflicted  in  this  way  to  such  an  extent 
that  new  neighbours  who  settled  in  an  adjoining  house  thought 
the  noise  was  made  by  a  sick  dog,  and  made  a  humane  suggestion 
that  the  animal  should  be  put  out  of  its  pain.  And  yet  this 
lady  could  recite  long  dramatic  passages  of  poetry  and  prose, 
though  in  ordinary  conversation,  or  even  when  not  talking,  her 
bark  made  her  society  a  mixed  pleasure. 

Stammering  in  its  different  varieties  is  not  uncommon  in 
hysterical  patients.  Unhke  ordinary  stammering  which  comes  on 
in   childhood,  hysterical   stammering   may   develop    suddenly  in 


THE    NEUROSES  365 

adult  life.  Thus  in  a  hospital  nurse  aged  33,  who  stood  up 
sharply  and  knocked  her  head  against  a  mantel- shelf,  severe 
hysterical  hemiplegia  came  on  next  day,  and  stammering  some 
six  weeks  later,  lasting  for  several  months. 

Sensory  Symptoms. — These  are  of  greater  diagnostic  import- 
ance than  is  commonly  realised.  Pain  of  some  sort  occurs  in  nearly 
every  case  of  neurasthenia  and  in  many  cases  of  hysteria.  Unlike 
ordinary  pains,  which  are  generally  caused  by  some  peripheral 
irritation,  hysterical  and  neurasthenic  pains  are  entirely  central 
in  origin — psychalgia — and  should  really  be  classed  as  halluci- 
nations. But  in  every  case  we  must  be  careful  to  see  and  to 
examine  the  painful  spot,  and  to  exclude  peripheral  irritation, 
before  labelUng  any  pain  as  hysterical  or  neurasthenic. 

Hysterical  pains  may  be  referred  to  any  part  of  the  body ;  but 
they  are  especially  common  in  certain  situations.  For  example, 
hysterical  headache  is  often  of  the  "  clavus "  type,  which  is  a 
boring  pain  locaHsed  to  one  small  spot  on  the  skull.  Occipital 
headache  is  particularly  common,  so  is  hemicrania.  Pains  in  the 
spine  may  simulate  those  of  organic  disease.  Pain  in  the  breast 
— mastodynia — or  in  the  joints  may  lead  to  difficulties  in  diagnosis. 
It  is  only  by  careful  local  and  general  examination,  reveaUng  the 
presence  of  other  hysterical  stigmata  and  the  absence  of  signs 
of  structural  disease,  that  we  can  avoid  errors.  Cases  have  been 
known  in  which  amputations  have  been  performed  for  hysterical 
joint-pains.  Some  time  ago  I  saw  a  young  lady  who  had  already 
had  one  toe  removed  by  a  surgeon,  but  the  pain  recurred  in 
another  toe,  and  the  case  was  undoubtedly  hysterical. 

Closely  related  to  these  pains  are  the  areas  of  hysterical  hyper- 
(Bsthesia,  and  especially  of  hyperalgesia  or  excessive  tenderness. 
Pain  on  pressure  over  certain  spots,  whether  such  pain  be  functional 
(hysterical  or  neurasthenic)  or  organic  in  origin,  has  occasionally 
to  be  differentiated  from  the  simulated  tenderness  of  a  malingerer. 
In  such  cases  Mannkopfs  sign  is  valuable.  This  consists  in  a  change 
in  the  pulse-rate  whilst  the  painful  spot  is  being  pressed  on — 
usually  a  temporary  acceleration  of  from  10  to  30  beats  per  minute. 
This  is  common  in  functional  cases.     Sometimes,  on  the  other  hand, 


366  NERVOUS   DISEASES 

the  pulse  is  slowed,  especially  in  cases  of  scars  from  organic  injuries.^ 
In  cases  of  malingering,  however,  no  alteration  in  the  pulse-rate 
is  produced.  Universal  hypersesthesia  is  rare.  We  also  meet  with 
cases  of  hemi-hypergesthesia.  More  usually  this  excessive  tenderness 
is  circumscribed  in  small  areas — little  islands  of  skin  or  subjacent 
tissues  of  the  head,  trunk,  or  limbs.  Sometimes  the  tenderness  is 
cutaneous  and  elicited  by  gentle  stroking  of  the  skin ;  sometimes 
it  is  subcutaneous,  and  only  elicited  on  deeper  pressure. 

Such  tender  points  are  chiefly  situated  in  the  vertebral,  infra- 
mammary,  epigastric,  and  inguinal  regions,  and  except  when 
mesial,  are  more  frequently  left-sided  (except  in  left-handed  people, 
in  whom  they  are  more  commonly  right-sided).  Tender  points  are 
less  common  on  the  head,  and  rarest  on  the  Hmbs.  Graves  ^  has 
directed  attention  to  the  frequent  presence,  in  hysterics  of  either 
sex,  of  hyperalgesia  to  pin-pricks  together  with  tactile  anaesthesia, 
confined  to  the  nipples  and  their  areolae. 

Of  all  the  tender  spots,  that  in  the  left  inguinal  region  is  per- 
haps the  commonest.  From  some  supposed  connection  with  the 
ovary,  it  has  been  called  "  ovarian  "  tenderness,  but  the  symptom 
is  as  frequent  in  male  hysterics  as  in  females,  so  that  the  term 
is  a  misnomer.  Moreover,  in  this  connection,  Steinhausen  ^ 
examined  500  healthy  soldiers — males,  not  Amazons — and  found 
that  in  no  less  than  88  per  cent,  brisk  pressure  in  the  inguinal 
region  on  either  side  produced  a  reaction  of  some  sort,  the  pheno- 
mena being  either  sensory  (unpleasant  tickhng  or  pain),  motor 
(hardening  of  abdominal  muscles,  various  reflex  and  protective 
movements),  psychical,  or  vaso-motor  and  sympathetic  (dilatation 
of  pupils).     And  yet  there  was  not  a  single  ovary  amongst  them. 

These  tender  points  may  be  associated  not  merely  with  pain, 

but  with  so  much  disturbance  as  to  be  actually  hysterogenic.     This 

does  not  mean  that  they  induce  hysteria— the  hysteria  is  already 

present.     It  means  that  pressure  on  such  a  spot  induces  a  hysterical 

fit  or  paroxysm.     The  best-known  hysterogenic  area  is  in  the  left 

^  Hudovernig,  Newrolog.  Centralhl.,  1910,  s.  408. 
^  Journal  of  Nervous  and  Mental  Diseases,  October  1905. 
^  Steinhausen,   Uebzr  die  physiologische  Grundlage  der  hysterischen  Ovarie. 
Deutsche  Zeitsch.  f.  Nervenheilk.,  xix.  s.  369. 


THE    NEUKOSES  367 

inguinal  region,  but  such  areas  may  be  an5rw]iere.  I  know  of  one 
patient  who  had  a  hysterogenic  spot  in  one  axilla  and  who  wore 
a  sort  of  truss  over  it,  to  prevent  accidental  pressure. 

Sometimes  deeper  pressure  on  the  hysterogenic  spot  or  else- 
where may  arrest  a  hysterical  fit  when  in  progress.  Areas,  pressure 
on  which  causes  cessation  of  the  paroxysms,  are  called  Jiystero- 
frenic.  The  inguinal  region  is  the  best  known  of  these.  Strong 
faradism  over  the  inguinal  region  will  stop  most  hysterical  fits  ; 
so  also  will  a  hypodermic  injection  of  apomorphine  with  its 
resultant  vomiting. 

Hysterical  hypersesthesia  may  also  affect  the  special  senses,  so 
that  there  may  be  hyper-sensitiveness  of  smell,  vision,  hearing, 
or  taste.  This  is  less  common  than  loss  or  diminution  of  special 
senses,  to  which  we  shall  refer  later.  I  had  for  some  time  under 
my  care  a  patient  who  could  not  tolerate  bright  hght,  especially 
if  the  room  had  a  blue  wall-paper.  He  preferred  to  stay  in  a 
darkened  chamber  ;  or  if  the  blinds  were  up,  he  shaded  his  eyes 
with  his  hand.  After  some  weeks  of  treatment,  he  completely 
lost  this  photophobia. 

In  rare  cases  an  actual  enlargement  of  the  visual  field  has 
been  observed,  generally  in  one  eye  only.  Thus,  in  a  soldier  with 
hysterical  wry-neck  and  ansesthesia  of  one  side  of  the  body,  the 
visual  field  on  the  non- anaesthetic  side,  when  measured  with  the 
perimeter,  was  much  larger  than  in  a  normal  individual. 

Hysterical  ancesthesia  is  extremely  common,  and  is  of  the  greatest 
diagnostic  value.  A  degree  of  anaesthesia  exists,  I  am  convinced, 
in  the  overwhelming  majority  of  hysterical  cases,  except  those 
occurring  in  childhood.  Some  time  ago  I  looked  through  my  notes 
of  63  consecutive  cases  and  found  that  anaesthesia  was  present  in 
50  and  absent  only  in  12.  The  remaining  case  of  the  series  had 
unilateral  hjrperaesthesia. 

Hysterical  anaesthesia  is  usually  unnoticed  by  the  patient  her- 
self, and  only  discovered  on  examination  by  the  physician.^     Some- 

^  Babinski  considers  that  hysterical  ansesthesia  is  mainly  the  result  of 
suggestion  by  the  examining  physician.  With  this  view  I  cannot  agree. 
Many  patients  who  are  highly  susceptible  to  suggestion  have  no  ansesthesia. 
Moreover,  undoubted  cases  of  hemi-ansesthesia  have  been  known  to  develoj) 


368  NEEVOUS    DISEASES 

times,  however,  the  patient  complains  of  actual  numbness,  and 
this  is  chiefly  in  cases  where  the  affected  Umb  has  motor  paralysis 
as  well,  so  that  her  attention  is  called  to  it. 

Janet  showed  an  ingenious  method  of  demonstrating  that 
in  some  cases  of  hysterical  anaesthesia,  sensory  impulses  really 
reach  the  brain-centres,  though  the  patient  does  not  consciously 
perceive  them.  Taking  a  case  of  complete  hemi-ansesthesia  he 
makes  the  patient  shut  her  eyes,  and  tells  her  to  say  "  Yes  " 
each  time  she  feels  a  touch  or  prick,  and  to  say  "  No  "when  she 
does  not  feel  it.  In  certain  cases  the  patient  not  only  says  "  Yes  " 
every  time  she  is  touched  on  the  normal  side,  but  also  says  "  No  " 
every  time  she  is  touched  upon  the  anaesthetic  side.  This  is 
pathognomonic  of  hysteria. 

Cutaneous  anaesthesia  in  hysteria  may  be  complete  or  partial 
in  degree,  or  it  may  be  dissociated.  Diminution  or  loss  of  painful 
sensations  is  even  commoner  than  tactile  anaesthesia.  Maiiy  of 
the  mediaeval  witches  were  simply  hysterics.  Their  hysterical 
analgesia  (sigillum  diaboli)  was  usually  demonstrated  by  sticking 
pins  into  them,  and  if  an  analgesic  area  was  discovered,  they  were 
promptly  thrown  into  the  nearest  pond  or  stream.  If  they  sank 
and  were  drowned,  their  innocence  was  estabhshed ;  but  if  they 
floated,  it  was  additional  evidence  of  guilt. 

Whatever  be  its  degree  of  intensity,  hysterical  anaesthesia 
never  maps  out  an  individual  nerve-area  such  as  that  of  the  radial, 
median,  ulnar,  or  external  popUteal.  Its  commonest  distribution 
is  a  hemi-ancBsthesia  (27  out  of  50  cases)  which  is  mostly  left-sided, 
except  in  left-handed  patients.  It  is  a  remarkable  fact  that  a 
hysterical  patient  never  suffers  any  physical  disability  owing  to 
the  existence  of  anaesthesia,  no  matter  how  profound.  Unlike  a 
patient  with  organic  anaesthesia,  the  hysteric  never  cuts  or  burns 
herself  unconsciously  in  an  anaesthetic  area. 

Hysterical   hemi-anaesthesia,  including  the   accessible    mucous 

membranes  of  the  eye,  nose,  mouth,  pharynx,  vagina  and  rectum, 

is  usually  accurately  bounded  by  the  middle  line  ;    but  not  always. 

before  any  medical  examination  had  taken  place,  the  anaesthesia  being  dis- 
covered accidentally  either  by  the  patient  or  by  some  lay  observer.  (See  a 
case  by  S.  A.  K.  Wilson,  Brain,  1911,  p.  320.) 


THE    NEUROSES 


369 


b'lG.  201.— Various  types  of  hysterical  ansesthesia.  Dotted  areas  indicate  slight 
sensory  loss,  shaded  areas  more  severe  impairment,  and  black  areas  total  loss 
of  sensation. 


2  A 


370 


NERVOUS   DISEASES 


HorlS 


N0¥Z6 


Fig.  202. — Case  of  hysterical  paralysis  in  a  girl  aged  17,  showing 
progressive  improvement  in  the  anesthesia. 


THE    NEUROSES 


371 


It  may  either  extend  farther  over  and  encroach  on  the  non-anses- 
thetic  side,  or  it  may  leave  certain  areas  with  normal  sensation, 
even  on  its  own  side,  especially  the  head,  the  nipple,  and  the 
genitals,  as  may  be  seen  from  the  charts  (Figs.  201  and  202). 

Bilateral  universal   anaesthesia  is  rare  (see    Fig.  84,    p.   198), 
We  generally  find,   somewhere  or  other,  one  or  more  islands  of 


Fig.  203. — Case  of  hysterical  paralysis  in  a  left-handed  patient, 
showing  progressive  improvement  in  anaesthesia. 

normal  sensation,  or  even  of  hyper-sensitiveness.  Pharyngeal 
anaesthesia  is  one  of  the  commonest  hysterical  stigmata.  It  is 
not  necessarily  accompanied  by  loss  of  the  pharyngeal  reflex. 

In  many  cases  the  anaesthesia,  though  unilateral,  is  more  marked 
on  the  face  or  limbs  than  on  the  trunk.  It  may  affect  special 
levels  of  a  Hmb  (knee,  elbow,  or  shoulder),  or  it  may  stop  abruptly 
at  some  horizontal  line  (shoe,  sock,  stocking,  mitten,  glove,  sleeve). 


372 


NERVOUS    DISEASES 


This  "  segmental "  ancesthesia  sometimes  occurs  in  association  with 
hemi-ansesthesia  (10  out  of  50  cases)  or  by  itself  (12  out  of  50)  on 
one  or  both  sides  (Figs.  203  to  205). 

The  mode  of  onset  and  disappearance  of  hysterical  anaesthesia 
is  interesting.  Sometimes  the  anaesthesia  comes  on  gradually,  and 
the  patient  is  unconscious  of  the  defect.     In  other  cases  it  occurs 


Fig.  204. — Case  of  hysterical  hemiplegia,  showing  variations  in 
anaesthesia. 

suddenly,  especially  after  a  hysterical  fit,  and  the  patient  is  then 
more  likely  to  notice  her  "  numbness." 

We  seldom  have  the  chance  of  watching  the  onset  of  hysterical 
anaesthesia,  but  we  may  often  study  its  mode  of  disappearance, 
and  Figs.  202  to  205  show  charts  of  several  cases  of  hysterical 
anaesthesia  in  various  stages  of  recovery.  Unlike  organic  anaes- 
thesia, which,  if  it  recovers,  fades  gradually  all  over  the  recovering 
area,  hysterical  hemi-anaesthesia  may  suddenly  fade  to  segmental 


THE    NEUROSES 


373 


(Fig.  202),  and  segmental  anaesthesia  recedes  by  jumps  from  a 
higher  to  a  lower  level,  bounded  usually  by  an  "  amputation  line  " 
drawn  transversely  across  the  hmb.  Sometimes  it  relapses  tempo- 
rarily to  its  old  level  before  resuming  its  progress  towards  recovery 
(Figs.  203  and  204).  More  rarely  it  clears  up  first  at  the  periphery. 
AncBstJiesia  of  Special  Senses. — Most  cases  of  hysterical  anses- 
ihesia  also  have  diminution  or  loss  of  the  special  senses — smell. 


Fig.  205. — Case  of  hysterical  paraplegia  with  anesthesia  in  a  girl  aged  19, 
showing  progressive  improvement. 

vision,  taste,  and  hearing — generally  unilateral  and  on  the  same 
side  as  the  cutaneous  anaesthesia,  rarely  on  the  opposite  side. 
This  combination  of  unilateral  affection  of  special  senses  and  of 
cutaneous  sensation  is  pathognomonic  of  hysteria,  and  does  not 
occur  in  organic  disease. 

The  affection  of  vision  in  hysteria  is  not  a  hemianopia  such  as 
we  often  get  in  organic  hemiplegia.     It  is  a  concentric  contraction 


374 


NERVOUS    DISEASES 


of  the  whole  visual  field,  as  will  be  seen  from  the  accompanying 
perimetric  charts  (Fig.  206).  It  is  more  marked  in  one  eye 
than  in  the  other — "  crossed  amblyopia  " — the  smaller  field  being 
on  the  hemi-ansesthetic  side,  usually  the  left. 

The  colour-fields  are  also  contracted,  but  in  a  different  order 


Bight  homonymous  hemianopia. 

Fig.  206.— Visual  fields  from  cases  of  hysterical  and  organic  hemiplegia 
respectively,  in  which  vision  was  affected. 

to  that  which  occurs  in  organic  optic  atrophy.  In  hysteria  the 
blue  field  diminishes  first  and  the  red  last  of  all,  whereas  in 
organic  atrophy  the  red  field  is  usually  first  affected. 

Sometimes,  when  charting  the  visual  field  of  a  hysterical  patient, 
we  notice  that  the  field  becomes  progressively  smaller  and  smaller. 


THE    NEUROSES 


375 


as  we  continue  our  examination,  so  that  our  perimetric  outline 
has  a  lielicoid  or  spiral  shape  (Fig.  207).  This  form  of  perimetric 
tracing  does  not  occur  in  organic  disease. 

Sometimes  we  have  hysterical  blindness  or  apparent  amaurosis 
in  one  eye,  and  yet  by  means  of  prisms  we  may  produce  a 
diplopia,    which  in  organic  cases  would  be  impossible.      In  very 


LEFT. 


Fig.  207. — Helicoid  contracbion  of  visual  fields  in  a  case  of  hysteria. 


rare  cases  complete  bilateral  hysterical  blindness  has  been 
observed. 

Space  does  not  permit  us  to  discuss  the  other  peculiarities  of 
hysterical  eye-affections  and  of  hysterical  loss  of  smell,  taste,  and 
hearing,  but  we  may  mention,  in  passing,  that  complete  bilateral 
loss  of  taste,  as  Hughlings  Jackson  pointed  out,  is  practically 
always  hysterical. 

Hysterical  Parcesthesia,  or  Perversion  of  Sensation. — In  some 
cases  of  hysteria  a  touch  on  one  hmb  or  one  side  of  the  body  is 
felt  by  the  patient  at  the  corresponding  spot  on  the  opposite  side — 
allocheiria  (Obersteiner).  In  another  variety,  of  which  I  have  seen 
an  example,  a  touch  on  the  radial  border  of  the  limb  was  felt  on 
the  ulnar,  and  vice  versd.  Haphalgesia  (Pitres)  is  the  term  used 
when  intense  pain  is  caused  by  touching  the  patient  with  certain 


376  NERVOUS    DISEASES 

substances,  such  as  metals,  which  normally  should  only  cause  a 
tactile  sensation. 

Parsesthesia  may  also  affect  the  special  senses,  as,  for  example, 
in  monocular  diplopia  or  polyopia,  which  is  always  hysterical. 
M*cro^s*a,  where  everything  looks  very  minute,  and  macro^JS*^,  where 
surrounding  objects  seem  gigantic,  are  both  frequently  hysterical. 

Motor  Phenomena. — These  may  be  subdivided  into  irritative 
and  paralytic.  Amongst  the  irritative  phenomena,  the  most 
striking  are  the  so-called  hysterical  fits  or  paroxysms.  Hysterical 
fits  vary  enormously  in  type  and  in  severity,  from  a  simple  emo- 
tional outburst  of  uncontrollable  laughing  or  crying,  accompanied 
perhaps  by  the  hysterical  "  globus  "  or  "  ball  in  the  throat,"  to  the 
most  prolonged,  dramatic  and  violent  muscular  movements,  together 
with  apparent  unconsciousness. 

One  variety  of  hysterical  fit  is  sometimes  mistaken  for  epilepsy, 
and  there  is  all  the  greater  liability  to  make  this  mistake  since  the 
fit  is  generally  over  before  we  reach  the  patient,  and  we  are 
dependent  for  our  information  upon  the  accounts,  more  or  less 
accurate,  of  unskilled  witnesses.  But  if  the  physician  is  lucky 
enough  to  be  present  during  a  fit,  there  is  seldom  any  difficulty 
in  diagnosis.  Thus,  for  example,  the  patient  never  hurts  herself 
in  falling ;  there  is  no  stertorous  breathing ;  her  face  is  not  livid, 
nor  does  she  bite  her  tongue  as  in  epilepsy  ;  she  may,  however,  bite 
her  lips  or  snap  at  the  fingers  of  the  bystanders.  She  never 
empties  the  bladder  or  rectum  during  the  fit ;  her  eyes  are  gener- 
ally tightly  closed,  and  if  the  physician  tries  to  open  them,  the 
patient  actively  resists.  A  hysterical  fit  is  not  followed  by  coma 
and  hardly  ever  by  vomiting. 

But  we  must  remember  that  sometimes  we  have  hysterical  fits 
which  are  post-epileptic — i.e.  which  immediately  succeed  an  attack 
of  true  epilepsy.  The  antecedent  epileptic  fit  in  such  cases  is 
usually  of  the  "  petit-mal "  type,  consisting  perhaps  in  a  mere 
transient  pallor  of  the  face,  with  momentary  loss  of  consciousness, 
and  then  passing  directly  into  a  hysterical  fit.  Therefore,  in  every 
case  it  is  important  to  inquire  very  carefully  as  to  the  precise  mode 
of  onset,  lest  we  overlook  a  case  of  combined  epilepsy  and  hysteria. 


THE   NEUROSES  377 

Charcot's  "  grande  hysterie,"  with  its  initial  period  simulating 
epilepsy  and  its  subsequent  phases  of  contortions,  kicking,  and 
struggling  (clownism),  passionate  attitudes  (opisthotonos,  cruci- 
fixion attitude,  &c.),  and  delirium,  often  with  hallucinations  of 
animals,  is  less  common  in  this  country  than  in  France,  but  once 
seen,  it  is  a  magnificent  performance  and  can  never  be  forgotten. 
It  is  totally  unhke  any  kind  of  epileptic  or  organic  fit,  and  its 
diagnosis  is  easy.  It  may  last  from  a  quarter  of  an  hour  to  several 
hours  at  a  time.  This  "  status  hystericus  "  is  commoner  than  the 
"  status  epilepticus,"  but  the  patient  has  no  subsequent  stupor 
such  as  that  which  succeeds  a  severe  epileptic  fit. 

Amongst  other  varieties  of  fits,  to  which  we  can  only  briefly 
refer,  we  may  mention  catalepsy,  in  which  the  patient  suddenly 
becomes  speechless,  motionless,  and  stiff.  Sometimes  she  is 
conscious  all  through  the  fit,  at  other  times  she  is  in  a  dreamy 
mental  state,  Meanwhile,  if  the  hmbs  be  passively  moved  into 
any  posture,  however  fantastic,  they  remain  fixed  there  hke  a 
doll's  limbs.  In  one  case  of  mine  the  patient,  a  woman  of  28, 
could  be  lifted  up  during  the  attack  by  the  head  and  heels  and 
laid  across  two  chairs  hke  a  log. 

Hysterical  trance  may  come  on  spontaneously,  or  may  succeed 
a  hysterical  paroxysm.  It  is  a  condition  in  which  the  patient 
appears  as  if  in  a  deep  sleep  ;  but  the  muscles  are  seldom  com- 
pletely relaxed,  and  we  may  observe  sHght  tremors  of  the  eyelids. 
In  more  severe  cases,  the  heart  and  respiration  may  become  so 
feeble  and  slow  that  the  condition  simulates  death.  Hysterical 
trance  may  last  hours,  days,  or  weeks  ;  and  several  cases  have 
been  authenticated  where  such  a  patient  has  been  buried  ahve, 
either  deliberately,  as  in  the  case  of  some  Indian  fakirs,  or  by 
accident  in  this  country.  Novehsts  know  this,  and  when  the 
heroine  is  thus  buried,  she  is  exhumed  in  the  last  chapter  by  the 
villain  for  the  sake  of  a  magnificent  diamond  ring  on  her  finger  ; 
whilst  her  finger  is  being  cut,  to  get  the  ring  off,  the  patient  awakes. 

We  can  only  mention  other  varieties,  such  as  somnambulism 
and  double  consciousness,  this  latter,  when  in  extreme  degree, 
being   a   condition  in   which    the   patient's    character    alternates 


378  NERVOUS    DISEASES 

between  normal  and  abnormal,  the  two  individualities  being 
mutually  unconscious  of  eacb  other,  but  each  one,  as  its  turn 
comes,  takes  up  the  thread  where  it  left  off  last. 

A  minor  degree  of  double  consciousness  can  be  demon- 
strated, by  a  simple  expsriment,  in  many  cases  of  hysteria  where 
there  happens  to  be  hysterical  angesthesia  of  the  upper  limb.  If 
in  such  a  case  we  screen  the  angesthetic  limb  from  the  patient's 
view,  she  does  not  feel  pin-pricks  or  touches  on  the  limb,  nor  does 
she  recognise  familiar  objects  when  placed  in  the  hand.  But  if  a 
pencil  be  placed  in  the  "  screened  "  hand,  it  is  grasped  in  a  position 
suitable  for  writing,  and  if  we  now  trace  a  letter  or  a  word  on  the 
back  of  the  angesthetic  hand  (the  patient's  attention  meanwhile 
being  diverted  by  another  observer)  this  letter  or  word  is  repro- 
duced in  writing,  entirely  unknown  to  the  patient's  consciousness. 
Analogous  sub-conscious  phenomena  can  be  demonstrated  in  many 
apparently  normal  people  by  means  of  a  small  wheeled  platform 
or  "  planchette  "  carrying  a  pencil. 

We  also  meet  with  a  hysterical  type  of  amhulatory  automatism 
where  the  patient  (more  often  a  man  than  a  woman)  has  attacks 
in  which,  without  adequate  motive,  he  has  a  sudden  and  irresistible 
impulse  to  wander  from  home.  He  makes  a  long  journey,  some- 
times undergoing  great  hardships  en  route.  Finally,  days,  weeks, 
or  even  months  afterwards,  he  suddenly  wakes  up  in  some  strange 
town  or  country,  entirely  unaware  of  how  he  got  there.  For 
example,  I  have  known  of  a  boy  who  disappeared  from  school  in 
this  way,  of  a  young  officer  who  deserted  from  his  regiment,  and 
of  a  business  man  who  left  his  wife  and  family,  all  these  cases 
without  any  adequate  cause.  These  cases  are  closely  related  to 
the  somnambulistic  stage  of  the  hypnotic  trance,  and  if  such  a 
patient  be  hypnotised  he  becomes  able  to  give  a  complete  account 
of  his  wanderings  from  the  moment  of  his  disappearance  to  the 
time  when  he  woke  up  and  "  found  himself."  The  diagnosis 
between  hysterical  and  post-epileptic  ambulatory  automatism,  to 
which  we  have  already  referred  (p.  69),  is  not  always  easy.  We 
should  carefully  inquire  for  evidences  of  epilepsy,  major  or  minor, 
we  should  look  for  the  presence  of  hysterical  stigmata  (though 


THE    NEUROSES  379 

even  in  hysterical  cases  stigmata  may  be  absent),  whilst  the  recon- 
struction of  the  "  lost  "  period  of  time  when  in  the  hypnotic  trance 
is  highly  suggestive  of  its  hysterical  origin. 

Various  localised  motor  disturbances  also  occur  in  hysteria  and 
psychasthenia.  Such,  for  example,  is  the  large  group  of  "tics"  and 
" habit  spasms"  which  we  have  already  studied  (p.  90).  A  true  tic  is 
essentially  and  primarily  a  psycho-motor  act,  either  an  emotional 
expression  or  a  movement  which  has  become  a  habit.  Of  these  tics, 
the  commonest  are  grimaces,  jerldngs  of  the  head,  trunk,  or  hmbs, 
and  tremors  of  various  parts,  rapid  or  slow.  Thus,  for  example,  a 
lady's  maid,  aged  46,  had  tonic  spasm  of  the  orbicularis  ocuK  on 
both  sides  (blepharospasm),  and  could  open  her  eyes  only  by 
opening  the  mouth  as  well.  Another  girl,  set.  19,  had  a  clonic  or 
jerking  paroxysmal  blepharospasm,  associated  with  "  humping  up  " 
of  one  foot.  Another  girl  of  19  had  rapid  "  twiddhng  "  movements 
of  the  left  thumb  and  fingers,  with  pronation-supination  movements 
of  the  forearm  and  a  pseudo-clonus  of  the  left  ankle.  Another 
girl,  aged  20,  who  previously  had  suffered  long  from  recurrent 
vulval  abscesses,  had  attacks  of  rapid  antero-posterior  movements 
of  the  pelvis.  Another  patient  had  rapid  violent  flexion-extension 
movements  of  the  left  elbow  whenever  a  thunderstorm  occurred, 
the  hand  meanwhile  dangling  loosely  at  the  wrist.  Such  cases  of 
locahsed  motor  disturbances  might  be  mulfciphed  almost  ad  infinitum. 

Hysterical  Paralysis  may  be  either  flaccid  or  spastic  in  type, 
and  may  affect  any  of  the  voluntary  muscles  ;  but,  unhke  paralysis 
due  to  organic  lesions,  it  never  attacks  a  single  muscle  nor  the 
muscles  supphed  by  a  single  nerve,  nor  are  the  electrical  reactions 
of  degeneration  ever  present.  A  further  point  about  hysterical 
paralysis  is  that  though  it  may  roughly  resemble  the  posture  of 
an  organic  paralysis,  it  never  does  so  with  accuracy ;  there  is 
always  some  point  of  difference  to  be  detected.  The  reason  for 
this  we  have  already  discussed  (p.  275). 

Let  us  study  one  example  each  of  hysterical  monoplegia,  of 
paraplegia,  and  of  hemiplegia. 

Fig.  208  is  that  of  a  nurse,  aged  32,  with  hysterical  monoplegia 
of  the  right  arm  of  eight  months'  duration,  in  whom  there  was 


580 


NERVOUS    DISEASES 


extreme  muscular  wasting  and  claw-hand.  The  paralysis  came  on 
after  a  strain  of  the  shoulder  in  lifting  a  heavy  patient,  and 
somewhat  resembled  a  lesion  of  the  brachial  plexus.  But  we 
observed  that  the  trapezius  was  paralysed,  and  that  the  whole 
scapula  was  displaced  downwards — unhke  an  organic  brachial- 
plexus  case,  in  which  the  arm  would  be  displaced  downwards  at 
the  shoulder-joint.     Moreover,  the  electrical  reactions  were  normal 


Fig.  208. — Hysterical  monoplegia  of  right  upper  limb,  accompanied  by 
muscular  atrophy,  but  without  changes  in  electrical  reactions. 


in  the  wasted  muscles,  and  there  was  a  "  glove  "  of  anaesthesia, 
unlike  the  "  root "  anaesthesia  of  an  organic  case.  The  patient 
was  treated  for  several  weeks  by  battery  and  massage,  without 
effect  at  first,  but  the  result  proved  our  diagnosis  to  be  correct, 
for  at  a  reHgious  meeting  she  was  suddenly  cured. 

Figs.  198  and  199  are  from  a  case  of  hysterical  flaccid  paraplegia 
of  fourteen  years'  duration  in  a  woman  of  37,  which  at  first  sight 
might  be  mistaken  for  a  cord-lesion  with  muscular  atrophy  and 
anaesthesia.      But  the  anaesthesia  was  of  the  "stocking"   type, 


THE    NEUROSES 


381 


tlie  reflexes,  deep  and  superficial,  and  the  electrical  reactions 
were  normal,  the  sphincters  were  unaffected,  and  there  were  no 
bed-sores  ;  and  the  result  of  six  weeks'  isolation  and  massage  was 
to  restore  the  power  of  walking  (Fig.  200). 

In  some  cases  of  hemiplegia  the  posture  is  sufficient  to  diagnose 
hysteria.    For  example,  in  the  patient  shown  in  Figs.  128  and  129 


Fig.  209. — Left-sided  hemi-glossic  spasm  in  a  case  of  hysterical  hemiplegia, 
showing  position  of  tongue  when  protruded. 

(p.  273),  instead  of  the  ordinary  posture  of  an  organic  case,  with  the 
upper  extremity  flexed  and  pronated,  the  lower  extremity  flexed  at 
the  hip,  extended  at  the  knee  and  ankle,  and  sHghtly  inverted,  there 
was  a  curious  posture  of  the  hand  and  foot  unlike  that  of  organic 
disease.  Moreover,  her  face  entirely  escaped,  in  spite  of  the  severe 
paralysis  of  the  arm  and  leg ;  and  she  had  hemi-ansesthesia  and 
loss  of  special  senses  down  one  side,  a  combination  which  never 
occurs  in  organic  hemiplegia. 


382  NERVOUS    DISEASES 

The  face  and  tongue  are  rarely  affected  in  hysterical  hemi- 
plegia. But  in  certain  cases  we  may  find  instead  of  weakness, 
spasm  of  the  face  and  tongue  on  the  affected  side,  when  the  patient 
shows  the  teeth  or  protrudes  the  tongue.  This  hysterical  glosso- 
labial  hemi-S'pasm  is  rare,  but  Figs.  209  and  131  (p.  274)  are  good 
examples  of  the  condition. 

We  may  also  refer  to  "  Lasegue's  symptom "  (Nothnagel's 
"Seelenlahmung")in  which  a  patient  with  an  anaesthetic  limb  cannot 
move  it  when  the  eyes  are  closed,  but  is  able  to  move  it  when  she 
opens  her  eyes  and  looks  at  it.  Another  feature  worthy  of  mention 
is  hysterical  pseudo-ptosis.  In  organic  ptosis  due  to  lesion  of  the 
third  cranial  nerve,  there  is  always  a  compensatory  over-action  of 
the  frontalis  muscle.  But  in  hysterical  pseudo-ptosis  this  is  absent, 
and  the  condition  is  really  due,  not  to  paralysis  of  the.  levator 
palpebrse,  but  to  spasm  of  the  orbicularis  oculi  (see  Fig.  61,  p.  136). 

Before  leaving  the  motor  phenomena  of  hysteria,  it  may  be 
well  to  refer  to  the  gaits  of  hysterical  and  psychasthenic  patients, 
which  are  sometimes  most  peculiar. 

Astasia-ahasia  is  a  hysterical  condition  in  which,  although  the 
patient  can  move  his  legs  normally  when  lying  or  sitting,  he 
collapses  at  once  when  he  tries  to  stand  or  walk.  Children  are 
more  often  affected  than  adults.  A  boy,  aged  12,  had  this  symptom 
for  a  long  time,  but  was  cured  by  an  application  of  the  faradic 
wire-brush  to  his  spine.  One  patient,  a  doctor  aged  55,  used  to 
flourish  his  left  leg  in  the  air  and  bring  it  down  with  a  stamp 
Uke  that  of  a  unilateral  locomotor  ataxia.  The  phenomenon,  an 
ambulatory  tic,  was  so  dramatic  that  he  had  to  carry  a  stick  to 
beat  off  the  crowds  of  little  boys  who  studied  his  gait  in  the 
streets.  Another  patient  was  a  worthy  married  lady  who  every 
now  and  then,  when  walking,  sat  down  suddenly  on  the  ground, 
rolled  backwards  and  spread  out  her  lower  limbs  like  the  letter  V. 

Perhaps  the  commonest  hysterical  gait  is  a  dragging  gait,  in 
which  the  patient  trails  the  limb  helplessly  along,  often  scraping 
the  inner  border,  or  even  the  dorsum  of  the  foot,  on  the  ground 
(see  Fig.  139,  p.  283),  unlike  an  organic  hemiplegia  in  which 
the  outer  side  of  the  sole  is  dragged. 


THE    Nl:UROSES 


383 


Some  authorities  state  that  muscular  atrophy  does  not  occur 
in  a  hysterical  limb.  But  this  is  not  accurate,  for  in  certain 
rare  cases,  one  of  which  is  shown  in  Fig.  208,  we  may  meet  with 
profound  atrophy.  But  this  atrophy  is  due  to  disuse  and  is  not 
associated  with  the  electrical  reactions  of  degeneration. 

Contractures  of  the  most  pronounced  type  may  be  met  with 


Fig.  210. — Hysterical  contracture  of  the  left  hand  and  elbow,  following 
an  injury  to  the  elbow. 

in  hysterical  paralysis.  But  here,  again,  they  always  differ  in 
some  respect  from  those  of  organic  cases.  Fig.  210  is  the  photo- 
graph of  a  soldier,  aged  32,  whose  horse  rolled  on  him  at  the  Tugela, 
and  who  afterwards  developed  a  stifi  left  arm,  flexed  at  the  elbow 
and  wrist,  and  with  the  thumb  and  index  finger  held  stiffly  parallel. 
A  study  of  the  reflexes  is  of  great  diagnostic  importance  in 
every  case  of  hysteria.  The  deep  reflexes  may  be  normal  or 
exaggerated,  but  in  pure  hysteria  they  are  never  lost,  although 
sometimes  they  may  be  "concealed"  by  the  presence  of  mus- 
cular spasm.  True  ankle-clonus  does  not  occur,  but  a  pseudo- 
ankle-clonus  is  often   met  with.      In   a    girl  of   19,  the   subject 


384  NERVOUS    DISEASES 

of  thread- worms  and  pruritus  ani,  this  pseudo -ankle-clonus  used 
to  come  on  spontaneously  when  sitting  or  standing  at  ease.  One 
can  often  distinguish  it  from  a  true  organic  clonus  by  the  pecuhar 
upward  start  of  the  foot  before  it  sets  ofi  on  its  first  downward 
push.     Further,  pseudo-clonus  is,  as  a  rule,  poorly  sustained. 

The  superficial  reflexes  are  often  diminished  especially  on  the 
anaesthetic  side.  The  plantar  reflex  in  hysteria,  if  present,  is 
always  of  the  normal  flexor  tj^e,  never  of  the  extensor  or  Babinski 
type.  A  persistent  extensor  plantar  reflex  only  occurs  in  cases 
of  disease  of  the  pyramidal  tracts,  and  in  infants  who  have  not 
learned  to  walk  and  in  whom  the  pyramidal  tracts  are  not  yet 
myelinated. 

The  pupil-reflex  to  light  is  never  lost  in  pure  hysteria, 
though  in  rare  cases  it  may  be  "  concealed  "  by  the  presence  of 
pupillary  spasm.  I  remember  one  case  of  fixed  dilated  pupils 
in  a  hysterical  woman,  but  this  was  due  to  the  taking  of 
belladonna  by  the  patient. 

As  to  the  bladder  and  rectum,  although  we  may  have  frequency 
of  micturition  in  hysteria,  we  never  have  true  incontinence.  Re- 
tention of  urine,  on  the  other  hand,  is  a  fairly  common  symptom. 
It  once  broke  out  as  an  acute  epidemic  in  a  school  for  young  ladies 
and  continued  until  the  doctor  judiciously  handed  over  the  duty ' 
of  catheterisation  to  a  female  nurse  of  mature  years.  The  symptom 
at  once  subsided  in  a  gratifying  manner. 

Visceral  and  Vaso-motor  Phenomena — It  is  important  to 
remember  that  hysteria  affects  the  sympathetic  nervous  system 
as  well  as  the  cerebro-spinal.  Let  us  refer  very  briefly  to  some 
of  the  visceral  and  vascular  phenomena. 

We  may  meet  with  abnormal  slowness  of  the  heart,  or  we  may 
observe  abnormal  rapidity  -with  palpitation,  chiefly  paroxysmal, 
constituting  a  variety  of  pseudo-angina,  especially  in  hysterical, 
or  neurasthenic  young  mothers  who  have  been  lactating  too  long. 
These  cases  are  easily  distinguished  from  true  angina  by  the 
absence  of  signs  of  organic  cardio-vascular  disease. 

In  the  digestive  system  we  meet  with  curious  hysterical  pheno- 
mena.    Aerophagy,  or  swallowing  of  air,  is  achieved  chiefly  by 


THE    NEUROSES  385 

gulping  movements  of  the  pharynx.  I  remember  a  httle  school- 
boy who  could  swallow  air  and  distend  his  abdomen  till  his 
waistcoat  could  not  be  buttoned.  We  are  all  familiar  with 
hysterical  dysphagia  or  spasm  of  the  oesophagus,  with  its  sudden 
intermissions  and  the  difficulty  experienced  equally  with  liquids 
and  with  solids,  in  which  nevertheless  a  large  stomach-tube  can  be 
easily  passed.  The  hysterical  "  globus  "  or  "  ball  in  the  throat," 
which  the  patient  tries  to  swallow,  is  an  emotional  phenomenon 
often  met  with  at  the  onset  of  a  hysterical  paroxysm.  Hysterical 
vomiting  has  always  to  be  excluded  in  gastric  disorders  of  young 
women.  It  is  often  associated  with  anorexia  nervosa,  where  the 
patient  will  take  hardly  any  food.  "  Fasting  girls,"  of  whom  we 
now  and  then  read  in  the  daily  press,  are  generally  examples  of 
this  kind  of  hysteria.  They  may  become  extraordinarily  emaciated, 
but  even  they  do  take  a  httle  food  now  and  then. 

Rhythmic  movements  of  the  stomach  or  intestine  accompanied 
by  curious  rumbhng  noises  are  sometimes  met  with.  The  commonest 
variety  is  the  intestinal,  and  at  dinner-parties  one  sometimes  hears 
these  noises  in  nervous  young  servant-maids  waiting  at  table.  Much 
less  frequently  we  hear  violent  gastric  borborygmi.  One  young 
girl  whom  I  saw  had  constant,  noisy  to-and-fro  gurghng  in  the 
upper  part  of  the  abdomen,  hke  a  steam-pump,  and  on  palpating 
the  abdomen  the  stomach  could  be  felt  rhythmically  contracting 
and  relaxing,  blowing  and  sucking  air  backwards  and  forwards. 
This  phenomenon  was  so  starthng  to  strangers  that  the  unfor- 
tunate girl  had  to  retire  to  her  own  room  if  friends  came  to  call 
on  the  family.  Somewhat  similar  abdominal  noises  in  another 
hysterical  patient,  a  lad  of  19,  were  apparently  produced  by 
spasmodic  contractions  of  the  diaphragm,  for  they  ceased  when 
he  drew  a  deep  breath  and  held  it. 

The  French  patient  who  earned  an  honest  hving  at  a  Parisian 
music  hall  by  making  musical  noises  with  his  anus  was  probably 
another  example  of  visceral  hysteria. 

We  must  also  bear  in  mind  the  pseudo-pregnancies  which  now 
and  then  occur,  in  which  spurious  enlargement  of  the  abdomen 
sometimes  goes  on  to  a  spurious  labour.     Then  "  parturiunt  montes, 

2  B 


386  NEEVOUS    DISEASES 

nascitur  ridiculus  mus  " — all  that  is  produced  being,  at  the  most, 
a  small  uterine  cast.  Phantom  abdominal  tumours  can  best  be 
difEerentiated  from  genuine  ovarian  or  uterine  enlargements  by- 
giving  an  anaesthetic,  when  the  abdomen  at  once  collapses. 

It  is  sometimes  more  difficult  to  diagnose  pseudo-appendicitis. 
Thus  one  patient  whom  I  saw,  aged  33,  had  had  her  abdomen 
opened  twice  in  different  London  hospitals  for  supposed  appendicitis, 
the  symptoms  being  those  of  recurrent  pain  and  tenderness  in  the 
right  iliac  fossa,  with  constipation  and  vomiting.  But  she  had 
also  right-sided  hemi-ansesthesia,  with  loss  of  special  senses  all  down 
that  side.  We  were  thus  led  to  suspect  the  hysterical  nature  of 
the  abdominal  symptoms,  and  accordingly  her  next  attack  was 
cured  by  sal  volatile,  without  laparotomy,  and  she  has  had  none 
since. 

Hysterical  diarrhoea  sometimes  occurs,  as  in  the  case  of  a  public 
speaker  who  was  often  attacked  in  this  awkward  way  just  when 
his  turn  arrived  to  address  the  audience. 

Spontaneous  haemorrhages  are  very  rare  in  hysteria,  and  no 
haemorrhage  should  ever  be  diagnosed  as  hysterical  unless  all  other 
causes  can  be  excluded.  But  a  certain  number  of  cases  of  pseudo- 
haemoptysis  and  pseudo-haematemesis  occur.  In  one  girl  whom  I. 
watched,  the  phenomenon  seemed  to  be  produced  by  sucking  of 
the  gums  ;  in  another  it  was  apparently  the  result  of  pharyngeal 
suction.  In  both  cases,  physicians  of  wide  experience  who  saw 
the  case  in  consultation  failed  to  discover  any  organic  cause  in  the 
chest  or  abdomen. 

Sometimes  a  limb  affected  by  hysterical  paralysis  or  anaesthesia 
may  show  abnormal  vasomotor  spasm,  so  that  if  pricked  or  cut  it 
bleeds  less  freely  than  normal. 

Secretory  phenomena  also  occur,  though  rarely,  as  for  example 
in  blood-stained  tears  or  blood-stained  sweat,  which  may  be 
unila,teral.  Polyuria  often  occurs  after  a  hysterical  fit,  whereas 
hysterical  anuria  or  suppression  of  urine  is  extremely  uncommon. 

Certain  skin  affections  occur  in  hysteria.  Cutaneous  haemor- 
rhages are  rare,  if  we  exclude  cases  of  voluntary  traumatism.  Bed- 
sores do  not  occur.     The  gangrenous  patches  described  as  hysterical 


THE    NEUROSES 


387 


gangrene  are  always  self-inflicted,  by  means  of  caustics  or  other 
methods  (see  Fig.  139,  p.  283).  Hysterical  blue  oedema  sometimes 
occurs,  especially  in  contractured  limbs  ;  it  usually  afiects  the  skin 
over  a  joint  and  produces  a  degree  of  cyanosis  and  swelling,  but 
this  swelling  does  not  pit  on  pressure.  Hysterical  oedema  may  last 
for  weeks  or  months.     It  generally  disappears  suddenly.     Thus  in 


-  Fig.  211. — Case  of  dermographism  in  a  hysterical  young  woman. 

a  case  recorded  by  Raymond,  it  suddenly  cleared  up  when  the 
patient  had  the  glad  stimulus  of  an  unexpected  legacy.  Dermo- 
graphism is  commoner  in  hysterics  than  in  normal  people.  Fig. 
211  is  an  excellent  example  in  a  girl  with  hysterical  tremor  of  the 
legs,  in  whom,  when  the  skin  was  stroked  with  the  finger-nail,  a 
white  raised  wheal  appeared  and  remained  for  an  hour  or  more. 


388  NEKVOUS    DISEASES 

This  "  factitious  urticaria,"  or  "  urticaria  scripta,"  unlike  ordinary 
urticaria,  does  not  itch. 

Hysterical  cough  is  very  common ;  it  is  usually  loud  and 
hacking,  going  on  all  day  and  ceasing  during  sleep.  It  is  not 
accompanied  by  expectoration,  and  is  commonest  in  young 
hysterics.  We  may  have  other  pecuHar  -modifications  of  respira- 
tion. Thus  in  a  girl  of  24  who  had  hysterical  fits,  expiration 
was  a  curious  grunting  noise  of  a  bigeminal  tj^e— two  grunts 
between  each  inspiration.  We  also  meet  with  paroxysmal  rapid 
breathing,  sneezing,  hiccup,  and  yawning.  One  girl,  aged  10,  the 
subject  of  hysterical  hemi-ansesthesia,  yawned  persistently  for  three 
weeks  during  her  waking  hours.  She  then  stopped  and  had  an 
attack  of  hysterical  mutism  lasting  for  two  months. 

When  hysteria  occurs  in  childhood  it  is  often  mono-sympto- 
matic and  the  ordinary  hysterical  stigmata  are  frequently  absent. 
Girls  are  much  more  frequently  affected  than  boys,  even  before 
the  age  of  puberty.  Perhaps  the  commonest  symptoms  of  hysteria 
in  childhood  are  astasia-abasia  and  hysterical  aphonia.  The  various 
forms  of  habit-spasm  are  common  in  young  psychasthenics. 

The  diagnosis  between  hysteria  and  organic  disease  is  some- 
times easy ;  in  other  cases  it  is  a  matter  of  extreme  difficulty. 
In  doubtful  cases  special  attention  should  be  paid  not  only  to  the 
psychical  symptoms  but  to  the  special  senses,  to  the  condition  of 
the  optic  discs,  to  the  type  of  anaesthesia  which  may  be  present, 
to  the  posture  of  the  hmbs  in  cases  with  motor  paralysis,  and  to 
the  condition  of  the  reflexes,  especially  the  plantar  reflex  and  the 
bladder  functions.  Further,  we  should  never  forget  that  hysteria 
and  organic  disease  may  coexist  in  the  same  case. 


CHAPTER  XXII 

ELECTRO-DIAGNOSIS  AND  ELECTRO-PROGNOSIS 

It  is  not  necessary  to  enter  into  a  full  discussion  of  the  various 
physiological  phenomena  produced  by  electrical  stimulation  of 
different  tissues,  still  less  to  discuss  the  nature  of  electricity  itself 
or  the  rationale  of  its  effects.  It  will  suffice  here  to  recall  a 
few  of  the  more  practical  points  in  the  physiology  of  electrical 
stimulation. 

Chnically,  electrical  stimulation  is  of  value  chiefly  in  the 
examination  of  muscles  and  of  motor  nerves.  Electrical  examina- 
tion of  sensory  functions  is  of  but  httle  practical  importance, 
except  perhaps  when  mapping  out  areas  of  loss  of  taste,  where 
a  mild  galvanic  current  is  an  excellent  gustatory  stimulus. 

For  diagnostic  purposes  the  three  most  important  forms  of 
electricity  are  the  faradic,  interrupted,  or  induced  current,  the 
galvanic  or  continuous  current,  and  the  vibrant  electricity,  which 
is  the  result  of  discharging  a  powerful  induced  current  through 
a  Crookes'  vacuum-tube,  producing  the  well-known  X-rays.  The 
apphcation  of  this  latter — so-called  skiagraphy,  though  of  great 
practical  importance,  does  not  specially  concern  the  neurologist. 
We  have  to  consider  more  particularly  the  faradic  and  the  galvanic 
currents. 

To  produce  the  galvanic  current,  we  employ  a  galvanic  battery 
(preferably  a  dry-cell  battery,  which  can  be  carried  about  without 
spilhng)  and  this  battery  must  have  sufficient  electro -motive  force 
or  voltage  to  overcome  the  resistance  of  the  skin,  which  is  a  bad 
conductor,  and  to  stimulate  the  muscles  and  nerves  underneath.  In 
cities  where  there  is  an  electric  hght  system  run  by  the  continuous 
current,  we  can  utihse  this  current  to  charge  an  accumulator  which 
can  be  carried  about,  or  we  may  use  the  current  direct  from  the 


390  NEEVOUS    DISEASES 

main,  provided  we  are  careful  to  reduce  tlie  voltage  sufficiently. 
This  is  accomplished  by  means  of  shunts,  resistances,  or  rheostats. 

Faradic,  or  induced  electricity,  is  obtained  by  induction.  In 
a  faradic  machine  there  are  two  coils  of  wire,  concentrically  placed 
— ^the  primary  coil  within  the  secondary.  When  a  galvanic 
current  passes  along  the  primary  coil,  there  is  produced,  at  the 
moment  of  closm'e  and  again  at  the  moment  of  opening  of  the 
primary  current,  an  instantaneous  faradic  shock  in  the  secondary 
coil,  no  shock  occurring  during  the  period  of  flow  of  the  primary 
current,  so  long  as  its  strength  remains  constant.  Within  the 
primary  coil  there  is  usually  a  bundle  of  soft  iron  wire,  which 
becomes  converted  into  a  magnet  when  the  galvanic  stream  flows 
round  the  primary  coil.  Now  a  magnet  pushed  within  a  coil  pro- 
duces an  instantaneous  faradic  or  induced  shock  in  that  coil ;  so  that 
as  the  soft  iron  is  alternately  magnetised  and  then  de-magnetised 
by  the  primary  coil,  we  have  the  effect  of  the  magnet  superadded 
to  that  of  the  primary  coil.  We  can  vary  the  strength  of  the 
faradic  shocks  in  the  secondary  coil  in  several  ways,  by  pulhng 
the  iron  bundle  in  or  out,  or  by  shding  a  cyhndrical  brass  shield 
between  the  primary  and  secondary  coils  (the  effect  on  the 
secondary  coil  being  greatest  when  no  shield  is  interposed),  or 
lastly,  by  having  the  secondary  coil  on  a  shding  sledge,  so  that  we 
can  pull  the  two  coils  apart.  This  last  is  the  best  and  most  deli- 
cate way  of  varying  the  intensity  of  the  faradic  shocks  in  the 
secondary  coil. 

We  apply  the  electrical  current  to  muscles  and  nerves  by  means 
of  metal  electrodes  of  various  sizes,  some  flat  and  disc-hke,  others 
with  rounded  bulbous  ends.  The  metal  surface  of  the  electrode 
should  be  covered  with  chamois-leather.  The  electrode  is 
screwed  on  to  a  holder,  which  must  have  a  contact-key  whereby 
we  can  interrupt  the  current  at  will.  The  chamois-leather  should 
be  soaked  before  use,  and  the  skin  should  also  be  well  moistened, 
in  warm  water  to  which  a  little  salt  has  been  added,  to  render  it  a 
better  conductor.  The  salt,  however,  spoils  the  leather,  which 
must  in  consequence  be  frequently  renewed. 

We  should  have  a  galvanometer  in  the  circuit  of  the  galvanic 


ELECTRO-DIAGNOSIS 


391 


392 


NERVOUS    DISEASES 


current,  so  as  to  measure  tlie  strength  of  current  whicli  pene- 
trates the  tissues.  There  should  also  be  a  commutator  or  shdmg 
switch,  whereby  we  can  reverse  the  direction  of  the  current. 
The  galvanic  battery  should  be  fitted  with  a  collector  whereby 
we  can  switch  on  the  different  cells,  one  by  one,  gradually  in- 
creasing the  strength  of  the  current. 

In  testing  the  electrical  reactions   of  muscles,   one  electrode 


,M.  rectus  abdo- 
minis (Abdo- 
minal intereostal ' 
nerves) 


:M.  serrat.  inagn. 

M.  latissimus 
dorsi. 


M.  obliquas 
abdom.  extemus 

{Abdominal     ; 
intercostal  nerves) 

M.  transversus 
abdominis. 


Fig.  213.— Motor  Points  of  Abdominal  Wall.     (Erb.) 

should  be  placed  on  the  spot  we  desire  to  stimulate,  whilst  the 
other  is  placed  on  some  far-distant  "  indifferent  "  spot,  where  any 
muscular  contractions  that  may  occur  will  not  interfere  with  the 
part  we  are  observing.  Thus  the  indifferent  pole  may  be  placed 
on  the  back  of  the  neck,  or  on  the  front  of  the  abdomen,  or  the 
patient  may  sit  upon  it,  or  he  may  hold  it  in  the  opposite  hand. 
We  then  fix  our  attention  on  the  other  pole  which  we  are  watching. 
To  stimulate  isolated  nerves  or  muscles,  either  the  electrode  should 
be  a  small  one,  or  we  may  employ  the  edge  of  a  disc  electrode. 


ELECTRO-DIAGNOSIS 


393 


The  patient  must  be  placed  in  a  good  Mght,  so  that  we  can 
see  the  sKghtest  movement  of  the  muscle  we  are  examining.     Some- 


M.  deltoideus  (pos- 
terior half) 


Museulo-spiral  nerve 
M.  brachial,  antic. 

M.  supinator  long. 
M.  radial,  ezt  long. 
H.  radial,  est  brev. 


M.  extensor  digit,  f 
communis        I 

M.  extensor  indicia 


M.  abdnotor  poUic.  long 
M.  extensorpollio.  brev. 


M.  inteross.  dorsaL  ( 
I  et  U  \ 


M. triceps  (longhead) 


M.triceps  (outer  head) 


M.  extensor  carpi  ulnari 
M.  supinator  brevis 

M.  extensor  digiti  minimi 
M.  extensor  indicis 


extens.  poU.  long. 


M.  abduct  digit  min. 

M.  inteross.  dorsal. 
m  et  IV 


Fig.  214.— Motor  Points  of  Upper  Limb.     (Erb.) 


times  by  placing  our  finger  on  the  tendon  of  the  muscle,  we  can 
feel  a  contraction  too  faint  to  be  visible.  The  patient  should  be 
made  to  relax  all  the  muscles  of  the  region  which  is  under 
examination.     Before  applying  the  electrodes  to  the  patient,  we 


394 


NEKVOUS    DISEASES 


M.  triceps  (long  head) 

M.  triceps  (inner  head) 
Ulnar  nerve  I 


M.  flexor  carpi  nlDaris 

M,  flex,  digitor.  commun. 
profund. 


M.  flex,  digitor.  subliia. 
^digiti  n  et  III) 

M.  flex,  digit,  subl.  (digit, 
iadicis  et  minimi) 

Ulnar  nerve 


M.  palmaris  brev. 

M.  abductor  digiti  mio. 

M.  flexor  digit,  min. 

M.  opponens  digit,  min. 


Mm.  lurabricales 


M.  deltoidenq 
(anterior  half) 


Musculo-cutaneous 
nerve    - 


M.  bice^is 
brachii 

,  M.  brachi 
anticus 


■Median  nerve 
M.  supinator  longus 
M.  pronator  teres 
M.  flex,  carpi  radialis 

M.  flex,  digitor.  sublim. 

M.  flex,  polliois  longus 
Median  nerve 

M.  abductor  pollic.  brov. 
M.  opponens  pollicis 

M.  flex.  poll.  brev. 

M.  adductor  pollic. 


Fig.  215.— Motor  Points  of  Upper  Limb.     (Erb.) 


ELECTRO-DIAGNOSIS 


395 


sliould  make  it  an  invariable  rule  to  test  the  strengtli  of  the  current 
on  our  own  skin,  to  avoid  startling  him  by  too  violent  a  shock. 

Electro-Diagnosis. — We  should  commence  with  faradic  shocks. 
Ordinarily  these  are  produced  in  rapid  succession  by  a  vibrating 
Neef's  hammer,   "  making  "  and  "  breaking "  the   circuit  of  the 


Anterior  crural  nerve, 

[OMurator  mrve 
M.  peotinaeus 

M.  adductor  magnus 
M.  adduct,  longns 

M.  oruralia 

M.  vastus  internus 


M.  tensor  fasciae  latae 


M.  sartorius 


M.  quadriceps  femoris 
(common  point) 

M.  rectus  femoris 


M.  vastus  extemns 


Fig.  21G.— Motor  Points  of  Anterior  Thigh  Muscles.     (Erb. ) 

primary  coil.  If  these  are  too  painful  to  be  borne,  we  may  often 
overcome  the  difficulty  by  loosening  the  spring  of  the  Neef's 
hammer  and  making  and  breaking  the  primary  current  by  moving 
the  spring  with  our  finger.  This  produces  an  isolated  faradic 
shock,  each  time  we  press  the  spring  into  contact  with  or  remove  it 
from  the  screw.  Such  single  shocks  are  often  tolerated  by  a  patient 
who  cannot  bear  the  ordinary  series  of  shocks  in  rapid  succession. 
In  children,  however,  it  is  sometimes  impossible  to  get  the  patient 
to  submit  even  to  single  shocks,  and  it  may  be  necessary  in  them 


396 


NERVOUS    DISEASES 


to  give  a  general  ansesthetic,  in  order  to  make  an  accurate  electro- 
diagnosis. 

Whenever  possible,    we   should  compare  the  reaction  of  the 
suspected  muscles  with  that  of  other  muscles  which  are  healthy, 


M.  tibial,  antic, 
M.  exten3.  digit,  comm. 
Jong. 


M   peronaeus  brevis 


M.  extensor  hallucis 
long. 


Km.  interossel  dorsales 


Pero7ieal  nerve 

M.  gastrocnem.  (outer  head) 
M.  peronaeus  longus 


Eoleus 


M.  flexor  hallucis  long. 


M  extens.  digit,  comm. 
brevjs 


M.  alductor  digiti  min. 


Fig.  217.— Motor  Points  of  Leg.     (Erb.) 

preferably  the  corresponding  muscles  of  the  opposite  limb.  Of 
course,  when  the  disease  is  bilaterally  symmetrical,  this  is  im- 
possible. An  electrical  examination,  to  be  complete,  would  have 
to  include  observations  on  every  accessible  muscle  and  motor  nerve 
in  the  body ;  this,  however,  is  practically  unattainable,  and  we 
usually  content  ourselves  with  selecting  a  group  of  muscles  in  the 
affected  area  and  testing  each  muscle  carefully,  both  with  faradic 
shocks  and  with  the  continuous  current,  commencing  with  the 
faradic. 


ELECTRO-DIAGNOSIS 


397 


Faradic  Reactions. — Faradism  stimulates  a  muscle  most 
efficiently,  not  by  direct  action  on  the  muscle-fibres  but  tlirough 
the  motor  nerve.  To  stimulate  an  individual  muscle  by  faradism 
we   seek    for    the    place    where    the    nerve    enters    the    muscle. 


Sciatic  nerve 
M.  biceps  feui.  (long  head ) 
M.  biceps  fem.  (short  head) 


Peroneal  nerve 


M.  gastrocnem.  (outer  head; 


M.  soleus 


M.  flexor  hallucis  long^us — 


J    M.  glutaeas  maximas 


M  adductor,  magims 
M.  semitendinosus 
M.  semimem'branosus 


Posterior  tihial  nerve 

M.  gastrocnem. (inner  head) 
M.  soleus 


M.  flexor  digitor.  comm. 
longas 


Posterior  tibial  nerve 


Fig.  218.— Motor  Points  at  back  of  Thigh  and  Leg.     (Erb.) 

This  is  usually  a  well-defined  spot  known  as  the  "  motor  point " 
of  the  particular  muscle.  Faradism  appHed  at  such  a  "  motor 
point "  provokes  a  maximal  contraction  in  that  individual  muscle. 
The  positions  of  the  chief  "  motor  points  "  are  indicated  in  Erb's 
well-known  diagrams  (Figs.  212  to  218).  A  faradic  shock  of  a 
given  strength  produces  a  much  greater  effect  when  appHed   at 


398  NEEVOUS    DISEASES 

such  a  "  motor  point "  than  when  apphed  directly  over  an  in- 
different bundle  of  muscle-fibres. 

Besides  stimulating  individual  muscles,  we  can  stimulate  whole 
groups  by  applying  our  electrode  over  a  nerve-trunk,  such  as  the 
ulnar  or  musculo-spiral. 

In  testing  faradic  reactions  we  commence  with  feeble  shocks  and 
gradually  increase  their  strength  until  we  just  get  a  contraction 
of  the  muscle.  We  then  compare  this  contraction  with  that  pro- 
duced by  the  same  strength  of  shocks  apphed  to  a  healthy  muscle, 
preferably  the  same  muscle  of  the  opposite  limb,  if  available. 

Galvanic  Reactions. — The  galvanic  current  stimulates  a  motor 
nerve-fibre  at  the  moment  of  closure,  and  again  at  the  moment 
of  opening  of  the  current,  but  not  during  the  period  of  flow,  so 
long  as  the  strength  of  the  current  remains  constant.  In  the  case 
of  muscle-fibres,  galvanism  stimulates  them  at  closure  and  again 
at  opening,  and  even  throughout  the  whole  period  of  flow,  pro- 
vided the  current  be  strong  enough.  Even  when  a  nerve  is 
degenerated,  directly  applied  galvanism  is  still  able  to  produce 
contractions  in  the  muscle-fibres. 

The  "  folar  reactions  "  of  a  muscle  to  galvanism  are  of  great 
cHnical  importance.  Normally,  in  a  healthy  muscle,  when  we 
stimulate  it  with  a  galvanic  current,  not  too  strong,  we  get  a 
brisk  twitch  at  closure,  then  during  the  period  of  flow  the  muscle 
remains  relaxed  until  the  current  is  suddenly  opened,  when  we  may 
get  another  twitch  at  opening.  The  contraction  at  closure  is 
greater  if  we  stimulate  with  the  kathode  (negative  pole)  than  if 
we  employ  the  anode  (positive  pole).  This  is  expressed  by  the 
formula  KCC  >  ACC  (kathodal-closure-contraction  greater  than 
anodal-closure-contraction).  To  verify  this  cHnically  on  a  healthy 
muscle,  we  gradually  increase  the  strength  of  our  current  by 
means  of  the  collector.  Meanwhile,  we  make  an  occasional  double 
movement  of  the  commutator,  whereby  the  testing  pole  is 
suddenly  changed  from  kathode  to  anode  and  back  again.  Pre- 
sently, as  the  current  is  increased  in  strength  we  find  that  at 
one  position  of  this  double  movement  we  get  a  brisk  twitch  of 
the   muscle,   whilst  in  the    reverse  position  we  get   none.     The 


ELECTRO-DIAGNOSIS  399 

first  twitch,  in  a  healthy  muscle  always  appears  at  the  kathode. 
Then  if  the  current  be  still  further  increased,  a  twitch  appears 
at  both  phases  of  the  commutator,  but  the  kathodal  contraction 
remains  the  greater.  As  a  matter  of  convenience  it  is  best  to 
employ  a  current  just  strong  enough  to  give  KCC,  whilst  as  yet 
there  is  no  ACC.  Meanwhile  we  notice  on  the  galvanometer  the 
number  of  miUiamperes  of  current  which  are  required  to  produce 
the  earliest  twitch  at  closure. 

If  the  strength  of  the  galvanic  current  be  still  further  increased 
we  obtain  a  twitch  at  opening,  the  anodal  contraction  being  pro- 
duced first  and  the  kathodal  opening  contraction  last  of  all.  The 
order  of  appearance  of  these  different  contractions  in  a  healthy 
muscle,  as  the  current  progressively  increases  in  strength,  is  there- 
fore as  follows  :  KCC  >  ACC  >  AOC  >  KOC,  and  is  indicated  in 
the  following  ampHfication  of  the  same  facts  : — 


1. 

Weak  current 

.     KCC 

% 

Medium  current     . 

.     KCC 

ACC 

3. 

Moderately  strong  current 

.     KCC 

ACC 

AOC 

4. 

Very  strong  current 

.     KCC 

ACC 

AOC 

KOC 

Of  these  phenomena,  we  usually  concern  ourselves,  for  practical 
purposes,  only  with  the  first  two,  that  is,  with  the  contractions  on 
closure,  observing  whether  the  kathodal  closing  contraction  is  greater 
than  the  anodal  closing  contraction,  as  it  ought  to  be  in  health. 

To  recapitulate,  in  a  normal  nerve-muscle  organ  we  obtain  a 
good  contraction  on  faradic  stimulation,  while  to  galvanism  there 
is  a  brisk  twitch  on  closure,  KCC  being  greater  than  ACC. 

Abnormalities  in  Electrical  Reactions. — Sometimes  the  ex- 
citability of  the  nerve-muscle  organ  is  increased,  both  to  faradism 
and  to  galvanism.  This  condition  of  hyper- excitability  is  met  with 
most  typically  in  tetany,  where  both  nerve  and  muscle  are  too 
easily  thrown  into  contraction.  Somewhat  similar  is  the  so-called 
"  neurotonh "  reaction,  described  by  Marina  -^  in  certain  cases  of 
hysteria,  by  Remak^  in  patients  with  progressive  muscular 
atrophy,  and  by  Handelsman  ^  in  syringomyelia.  This  pheno- 
menon consists  not  only  in  excessive  excitabiHty  both  to  faradism 

1  Neurologisches  CentralUatt,  1896,  No,  17.  2  /jj-^L,  1896,  No.  13. 

=»  Ibid.,  1911,  s.  418. 


400  NERVOUS    DISEASES 

and  galvanism,  but  also  in  a  tendency  for  the  muscle  to  remain 
in  a  state  of  tetanus  for  10  to  30  seconds  after  the  stimulus 
has  ceased.  The  phenomenon  is  not  provoked  hj  stimulation  of 
the  muscle  itself,  but  only  by  excitation  of  the  nerve. 

We  sometimes  meet  with  simple  diminution  of  excitabihty,  both 
to  faradism  and  to  galvanism,  but  without  alteration  of  polar 
reactions — that  is  to  say,  KCC  remains  greater  than  ACC.  Such 
diminution  of  electrical  excitability  is  met  with  in  simple  arthritic 
muscular  atrophy,  in  the  atrophy  of  disuse  and  also  in  the  various 
myopathies,  whether  pseudo-hy]pertrophic  or  atrophic  in  t3^pe. 

Temporary  loss  of  faradic  excitability  occurs  in  myasthenia 
gravis,  though  not  in  every  case.  When  present,  the  myasthenic 
reaction  consists  in  the  fact  that  after  a  certain  number  of  faradic 
shocks,  the  muscle  gradually  reacts  less  and  less,  until  at  last 
it  shows  no  contraction  to  the  strongest  faradic  shocks.  We  wait 
a  few  minutes  and  then  test  again,  when  we  find  that  the  faradic 
excitability  has  reappeared,  but  can  again  be  exhausted  in  a 
similar  fashion.  The  galvanic  reactions  of  the  affected  muscles 
remain  unchanged  throughout  the  disease.  A  myasthenic  reaction 
can  also  be  produced  experimentally,  e.g.  in  the  frog's  muscles,  by 
poisoning  with  yohimbine.^  This  suggests  that  the  phenomenon 
is  toxic  in  origin. 

During  the  paroxysms  of  the  rare  disease  known  as  family 
'periodic  paralysis,  the  paralysed  muscles  are,  for  the  time,  totally 
inexcitable  either  by  faradism  or  by  galvanism.  In  the  intervals 
between  the  attacks  of  paralysis,  the  muscles  react  normally. 

The  myotonic  reaction  is  met  with  chiefly  in  Thomsen's  disease 
(myotonia  congenita),  but  has  also  been  observed  in  certain  types 
of  syringomyelia  accompanied  by  myotonia.  It  consists  in  the 
fact  that  on  faradic  stimulation  the  muscular  contraction  persists 
for  some  time  after  the  stimulus  has  ceased,  as  if  the  muscle,  once 
contracted,  cannot  relax.  Moreover,  in  this  disease  galvanic 
stimulation  of  the  muscle  produces  curious  wave-like  contractions, 
and  KCC  is  equal  to  instead  of  greater  than  ACC. 

Reactions  of  Degeneration. — By  far  the  most  important  modi- 

^  Gunn,  Rev.  of  Neurol,  and  Psychiat.,  1908,  p.  150. 


ELECTRO-DIAGNOSIS  401 

fication  of  electrical  reactions  is  the  condition  known  as  the 
"  reactions  of  degeneration,"  or  colloquially  as  R.D.  This  condition 
is  present  when  the  nerve-muscle  organ  has  undergone  degenera- 
tion, from  disease  or  destruction  of  the  spino-muscular  motor 
neurone.  As  a  result  of  such  a  lesion,  the  motor  nerve-fibre  dis- 
integrates within  a  few  days  and  loses  its  power  of  conducting 
impulses.  The  corresponding  muscle-fibre  undergoes  important 
changes ;  it  loses  its  fibrillar  or  anisotropic  element,  the  element 
which  contracts  with  a  brisk  twitch  and  can  be  stimulated 
with  a  faradic  shock ;  whilst  it  retains  only  its  sarcoplasm,  a  less 
excitable  element,  which  contracts  slowly  and  can  still  be  stimu- 
lated by  galvanism. 

In  a  typical  case  the  phenomena  are  as  follows  : — ^to  faradism 
there  is  no  response,  since  the  nerve  has  degenerated  ;  to  galvanism 
the  muscle-fibres  still  respond — ^in  fact  for  a  short  time  they  become 
hyperexcitable,  contracting  to  a  weaker  current  than  in  health. 
But  their  polar  reactions  are  altered.  The  anodal  contraction  on 
closure  is  now  equal  to,  or  greater  than  the  kathodal  (ACC  >  KCC). 
Moreover,  what  is  equally  characteristic,  the  response  of  the 
muscle  is  no  longer  a  brisk  twitch  ;  it  is  a  slow,  sluggish,  almost 
vermiform  movement.  If  a  nerve  be  divided,  the  reactions  of 
degeneration  do  not  appear  at  once.  It  is  only  after  some  ten 
days  or  so  that  they  develop.  Once  established,  the  reactions 
of  degeneration  persist,  unless  the  nerve  regenerates  and  re- 
estabhshes  a  connection  between  the  muscle  and  the  motor  nucleus. 
In  the  process  of  recovery,  voluntary  motor  power  reappears  before 
faradic  excitabihty  returns.  In  many  cases  recovery  does  not  take 
place  and  the  nerve-muscle  organ  remains  permanently  degene- 
rated, as,  for  example,  where  the  motor  nucleus  in  the  cord  or 
medulla  is  destroyed,  or  where  a  nerve-trunk  is  completely  divided 
and  its  ends  have  not  been  reunited. 

In  certain  cases  we  meet  with  fartial  or  incomplete  reactions  of 
degeneration.  These  consist  in  a  sluggish  contraction  to  galvanism, 
ACC  being  greater  than  KCC,  but  the  reaction  to  faradism  is  not 
lost,  but  only  diminished.  This  condition  indicates  a  less  severe 
injury  of  the  nerve-fibres  than  if  typical  R.D.  be  present. 

2  c 


402  NERVOUS    DISEASES 

Sometimes  we  liave  mixed  reactions,  where  some  fibres  of  a 
muscle  retain  their  normal  reactions  whilst  adjacent  fibres  have 
reactions'  of  degeneration.  This  is  best  exemplified  by  cases  of 
progressive  muscular  atrophy  where  degenerated  muscle-fibres  are 
interspersed  amongst  the  healthy. 

To  sum  up,  then,  the  presence  of  R.D.  always  indicates  a  lesion 
somewhere  in  the  lower  or  spino-muscular  motor  neurone.  We 
should  be  careful  to  wait  ten  days  or  a  fortnight  from  the  onset 
of  the  paralysis  before  giving  this  verdict,  inasmuch  as  we  have 
seen  that  it  takes  some  time  for  degeneration  to  become  estab- 
lished. R.D.  occur  in  lesions  of  peripheral  motor  nerves,  also  in 
gross  nuclear  diseases  such  as  acute  anterior  pohomyehtis,  haemor- 
rhage, or  thrombosis  in  the  anterior  cornua  or  motor  nuclei.  Mixed 
reactions,  on  the  other  hand,  are  found  in  progressive  muscular 
atrophy  and  in  bulbar  palsy,  where  the  nerve-cells  of  the  motor  nuclei 
are  picked  out  one  by  one,  leaving  adjacent  nerve-cells  unaffected. 

Electro-Prognosis.^ — In  many  paralyses  due  to  organic  lesions 
of  peripheral  motor  nerves  (of  which  the  commonest  instance  is 
^:hat  of  a  neuritis  of  the  facial  nerve),  it  is  of  importance  to  be  able 
to  estimate  not  only  the  degree  of  degeneration  which  has  occurred, 
but  also  the  prospects  of  recovery.  To  make  an  accurate  prognosis 
we  must  wait  at  least  ten  days,  and  preferably  a  fortnight,  before 
making  our  investigation,  so  as  to  allow  time  for  degenerative 
changes  to  have  occurred.  Electrical  examination  at  any  earlier 
date  is  practically  valueless  for  purposes  of  prognosis.  If,  after  a 
fortnight's  motor  palsy — say,  in  a  case  of  Bell's  paralysis — we  get 
typical  R.D.,  the  degeneration  of  the  nerve  is  severe  and  recovery 
will  not  commence  for  three  months  at  least,  possibly  not  for  a  year, 
and  the  patient  may  even  remain  permanently  paralysed.  And 
at  the  best,  if  recovery  does  occur,  it  will  probably  be  imperfect 
and  associated  with  some  contracture.  If  partial  R.D.  be 
present,  the  prognosis  is  less  grave  and  recovery  may  be  expected 
within  six  or  eight  weeks.  If  the  reactions  be  normal,  or  if  there 
is  simply  a  diminution  to  faradism  and  galvanism,  but  without 
polar  changes,  recovery  may  be  looked  for  in  from  three  to  six 
weeks,  or  even  sooner. 


CHAPTEll   XXIII 

THE   CEREBRO-SPINAL  FLUID 

The  cerebro-spinal  fluid,  is  secreted  by  the  ependyma  covering 
tlie  choroid,  plexuses.  The  amount  secreted  may  be  considerable. 
In  cases  of  cranial  or  spinal  injury  where  the  subarachnoid  space 
is  in  communication  with  the  surface,  as  much  as  2  to  4  litres  daily 
have  been  observed  to  escape.  In  some  patients,  as  St,  Clair 
Thompson  and  others  have  shown,  a  spontaneous  flow  of  cerebro- 
spinal fluid  occurs  through  the  cribriform  plate  and  drips 
constantly  from  the  nose. 

The  posterior  lobe  of  the  pituitary  body  pours  its  secretion 
through  the  hollow  infundibulum  into  the  cerebro-spinal  fluid  of 
the  third  ventricle.  Experiments  by  Gushing  and  Goetsch  ^  have 
demonstrated  that  normal  cerebro-spinal  fluid  contains  a  substance 
which  gives  the  same  reaction  as  extracts  of  the  pars  nervosa  itself. 
The  fluid  receives  various  products  of  metabolism  from  the  nerve- 
centres.  It  may  undergo  changes  in  lesions  of  these  centres  or  of 
their  meninges  ;  hence  the  clinical  importance  of  its  examination. 

In  the  adult,  the  spinal  cord  terminates  at  the  level  of  the  lower 
part  of  the  first  lumbar  vertebra.  Below  that  level  the  arachnoidal 
sac  extends  as  a  hollow  cavity  as  low  down  as  the  second  sacral 
vertebra  (see  Fig.  219).  There  is  thus  a  considerable  extent  of 
arachnoidal  cavity  devoid  of  spinal  cord,  occupied  simply  by  the 
roots  of  the  cauda  equina  and  by  the  cerebro-spinal  fluid  which 
bathes  them.  From  this  region  we  can  withdraw  cerebro-spinal 
fluid  without  risk  of  injury  to  the  spinal  cord.  In  order  to  do 
so,  we  enter  the  cerebro-spinal  cistern  from  behind,  somewhere 
between  the  laminse  of  the  second  lumbar  and  the  second  sacral 
vertebra. 

The  two  widest  inter -laminal  spaces  are  the  one  between  the 
third    and  fourth,  and    the    other  between  the  fourth  and  fifth 

^  Am.  J.  of  Physiology,  1910,  vol.  xxvii.  p.  60. 
403 


404 


NEEVOUS    DISEASES 


IZTh 


Direction  of 


lumbar  laminae.  Of  these  we  usually  select  the  space  between  the 
fourth  and  fifth  laminae,  because,  as  a  rule,  it  is  slightly  the  larger. 
These  two  inter-laminal  spaces  are  very  easily  found  as  follows  :  we 

draw  a  horizontal  Hne  across  the 
patient's  back,  at  the  level  of  the 
highest  margin  of  the  ihac  crests. 
This  hne  intersects  the  vertebral 
colunm  at  the  tip  of  the  fourth 
lumbar  spine.  We  make  our 
puncture  immediately  below  this 
spine  (Fig.  220). 

It  is  convenient  to  use  an  aU- 

glass    syringe    which    is    readily 

•  "^^umbar'"^  stcrihsable    on    which   to   mount 

5L      puncture      ^^    ^i^^^^,     which    should     be     of 

fairly  large  calibre.  The  needle 
itself  is  made  of  platinum  and 
iridium,  which  is  less  liable  to 
snap  and  can  also  be  boiled  with- 
out rusting,  unhke  a  steel  needle. 
It  must  be  long  enough  to  reach 
into  the  arachnoidal  sac,  and  yet 
short  enough  to  stop  short  with- 
in the  sac  without  penetrating  to 

Fig.  219.— (After  Raymond.)  Diagram  the    dura    on    the  far   side.     For 

of  lower  end  of  vertebral  column  and         .  •     ^  ^ 

its  relations  to  the  spinal  cord  and  thlS    purpoSe     the  most     Suitable 

Cauda   equina.     The    double-shaded  i         ,i       <•           n     •  i        .    o          ±.- 

portion  of  the  cord  is  the  conus  ter-  length  of  needle  IS  about  8  centi- 

minaiis,  with  which  the  filum  ter-  metres,  or  iust  over  three  inches, 
mmale  is  continuous.  •• 

As  to    the    patient's    posture 

during   the  operation  of   "thecal   puncture,"  he  may  be  lying  on 

a  bed  or  couch,  in   the  left  lateral  position,  with  the  knees  and 

shoulders   approximated.     But   it  is    better,  if   possible,  to  have 

him  sitting   on   a   low   seat,    stooping    well    forwards,    with    his 

knees  separated,  his  arms  hanging  loose,  and  his  hands  touching 

the  ground.     In  this  way  the  laminae  are  separated  to  their  utmost 

extent  (see  Fig.  220). 


THE    CEREBRO-SPINAL    FLUID 


405 


We  carefully  sterilise  the  skin  at  the  site  of  puncture  and  render 
it  anaesthetic  by  means  of  a  spray  of  ethyl  chloride.  The  operator 
places  his  left  index  finger  on  the  fourth  lumbar  spine  as  a  guide, 
and  with  liis  right  hand  pushes  in  the  needle,  about  half  an  inch 
below  and  half  an  inch  to  the  right  of  this  spot  (so  as  to  avoid  the 
dense  interspinous  ligament),  directing  the  point  of  the  needle 
horizontally  forwards  and 
a  little  inwards.  The  liga- 
mentum  subflavum,  deep  in, 
between  the  laminae,  is 
somewhat  resistant,  and  the 
needle  is  felt  to  be  checked 
here.  But  we  push  firmly 
on,  if  no  bone  is  struck, 
and  suddenly  the  needle 
penetrates  the  ligament  and 
dura-arachnoid  and  is  now 
in  the  arachnoidal  sac  (see 
Fig.  221).  If  we  strike  on 
a  lamina  instead  of  the 
hgament,  we  withdraw 
shghtly  and  try  a  point 
above    or   below. 

Sometimes  during  the  operation  the  patient  feels  a  sudden, 
sharp  pain  shooting  down  his  right  thigh  and  leg.  This  simply 
means  that  our  needle  has  touched  one  of  the  roots  of  the  cauda 
equina  en  route,  and  is  of  no  other  significance. 

We  now  detach  the  syringe  and  allow  the  cerebro-spinal  fluid 
to  escape  through  the  needle,  collecting  from  3  to  5  c.c.  in  a 
sterilised  test-tube.  It  is  better  not  to  employ  suction  by  the 
syringe,  unless  some  difficulty  be  experienced  in  getting  the  fluid 
to  run.  The  pressure  of  the  fluid  as  it  escapes  may  be  measured, 
if  desired,  by  means  of  a  rubber  tube  with  a  manometer  attached. 
Normally  the  fluid  trickles  out  slowly,  drop  by  drop.  The  first 
few  drops  should  be  discarded,  since  they  may  be  mixed  with  blood 
from  our  needle- wound  of  the  superjacent  tissues. 


Fig.  220. — Lumbar  puncture.     Fluid  drop- 
ping from  needle  into  test-tube. 


406 


NEKVOUS    DISEASES 


Occasionally  it  happens  that  even  when  we  have  successfully 
penetrated  within  the  ligamentum  subflavum,  no  fluid  will  flow. 
This  is  usually  due  to  blocking  of  the  needle  by  a  small  plug 
of  blood-clot  or  shred  of  muscle  or  connective-tissue,  during  the 
process  of  puncture.  Or  it  may  be  due  to  one  of  the  cauda 
equina  roots  floating  against  the  end  of  the  needle.  Such  con- 
ditions are  easily  rectified  by  passing  a  steriUsed  stilette  along  the 
needle,  to  clear  it.  Sometimes  it  happens  that  the  needle  pierces 
the  Hgamentum  subflavum  but  pushes  the  spinal  theca  in  front  of 
it,  so  that,  even  though  the  stilette  shows  the  needle  to  be  free  from 

Corrmwjii  IUccc  Arteries. 


■In/eriorVenay  Cavou. 


-Erector SpuvcLe^ . 


Fig.  221. — Horizontal  section  at  the  level  of  the  fourth  lumbar  vertebra, 
showing  the  relations  of  the  parts  concerned  in  thecal  puncture. 

obstruction,  no  fluid  comes.  In  such  cases  it  is  best  to  withdraw 
the  needle  and  puncture  at  the  next  space  above. 

Sometimes  the  intrathecal  pressure  is  increased,  so  that  the  fluid 
escapes  in  a  jet,  instead  of  drop  by  drop.  This  occurs  chiefly  in 
intra-cranial  tumours  and  in  the  various  forms  of  meningitis, 
although  even  in  these  conditions  an  increased  pressure  of  fluid 
in  the  lumbar  region  is  by  no  means  constant,  for  sometimes  in 
meningitis  there  is  occlusion  of  the  foramen  of  Magendie,  or  of 
the  foramina  of  Key  and  Retzius,  or  the  cerebellum  may  be 
partially  impacted  in  the  foramen  magnum,  cutting  off  the 
intra-ventricular  from  the  spinal  pond. 

The  fluid  may  be  accidentally  mixed  with  blood  from  the 
wounding  of    an  arachnoidal  vein  during  the  puncture ;    this  is 


THE    CEREBRO-SPINAL    FLUID  407 

an  accident  wliicli  cannot  be  foreseen.  In  most  cases  such  bleed- 
ing clears  up  after  a  few  seconds,  the  fluid  becoming  progressively 
clearer  and  clearer.  But  admixture  of  blood  also  occurs  in  cases  of 
pre-existent  subarachnoid  haemorrhage,  cerebral  or  spinal,  as  in  frac- 
ture of  the  skull,  intra-ventricular  haemorrhage,  or  in  trauma  of  the 
spinal  cord.  We  can  sometimes  distinguish  between  haemorrhage 
due  to  the  local  puncture  and  haemorrhage  which  results  from 
a  previous  intra-thecal  lesion.  We  do  this  by  centrifuging  the 
fluid.  In  local  haemorrhage  due  to  puncture,  the  blood  corpuscles 
fall  to  the  foot  of  the  centrifuge-tube,  leaving  the  superjacent 
fluid  clear  and  hmpid,  whereas  in  a  pre-existing  cerebral  or  spinal 
haemorrhage  the  fluid  (which  during  its  flow  is  equally  tinged 
from  start  to  finish,  and  generally  less  deeply  tinged  than  in  local 
haemorrhage),  remains  of  a  yellow  colour  even  after  centrifuging. 

The  withdrawal  of  a  small  quantity  of  cerebro-spinal  fluid  in 
most  cases  causes  the  patient  no  discomfort.  But  in  a  small  pro- 
portion of  cases  he  may  complain  of  severe  headache,  appearing 
an  hour  or  two  later,  and  lasting  perhaps  for  several  days.  This 
is  usually  in  patients  who  have  been  walking  about  as  usual  after 
the  puncture,  and  headache  can  generally  be  prevented  by  re- 
commending the  patient  to  rest  for  a  day  or  so,  or  at  least  to 
avoid  physical  exertion. 

Normal  cerebro-spinal  fluid  is  absolutely  colourless,  like  water. 
It  has  a  specific  gravity  of  1006  to  1008.  It  is  alkaline,  contains 
a  trace  of  serum-globulin  and  of  albumose,  and  also  a  substance 
which  reduces  Fehling's  solution  and  forms  glucosazone  crystals. 
Microscopically  it  contains  a  few  large,  flat,  endothelial  plates, 
and  perhaps  an  occasional  lymphocyte.     It  contains  no  organisms. 

The  Diagnostic  Significance  of  Cerebro-spinal  Fluid. — For 
diagnostic  purposes,  the  fluid  may  be  examined  in  various  ways. 

(1)  Physical  Characters. — Instead  of  being  clear  and  limpid 
like  water,  the  fluid  may  be  opalescent,  turbid,  cloudy,  or  even 
purulent,  as  in  some  cases  of  meningitis.  In  severe  jaundice  it 
has  been  observed  to  be  yellow  and  clear,  whilst  in  cases  of  recent 
haemorrhage  either  into  the  brain  or  cord,  as  we  have  mentioned, 
it  may  be  blood-stained.  In  haemorrhages  of  older  date,  say  a 
week  or  more,  the  fluid  may  be  of  a  clear  yellow  colour. 


408  NERVOUS    DISEASES 

In  cases  of  sudden  liemiplegia,  we  are  sometimes  in  doubt 
whetlier  the  lesion  is  ligemorrliage  or  thrombosis.  The  diagnosis 
between  these  two  conditions  may  be  very  difficult.  But  the 
treatment  of  the  two  is  diametrically  opposite.  In  a  case  of 
thrombosis  we  stimulate,  and,  if  necessary,  push  our  anti- 
syphilitic  remedies,  whereas  in  cerebral  haemorrhage  we  try  to 
lower  the  intra-cranial  blood-pressure  and  diminish  the  force  of 
the  heart.  If  in  a  doubtful  case  we  perform  lumbar  puncture 
and  obtain  blood-stained  fluid,  or  fluid  which  has  a  yellow  tinge 
even  after  centrifuging,  the  diagnosis  may  be  much  simplified. 
I  have  performed  lumbar  puncture  in  a  comatose  patient  moribund 
from  cerebral  thrombosis  and  obtained  normal  clear  fluid.  In 
traumatic  cases  it  is  of  great  value  in  indicating  the  presence  of 
intra-cranial  haemorrhage.  Cathcart  of  Edinburgh  ^  recorded  a 
case  in  which,  after  a  head  injury,  examination  of  the  cerebro- 
spinal fluid  helped  to  settle  the  diagnosis  of  intra-cranial  haemor- 
rhage. He  trephined,  tied  the  ruptured  artery,  and  saved  the 
patient's  life.  But  in  compound  fracture  of  the  skull  lumbar 
puncture  may  yield  nothing,  if  the  fluid  happens  to  be  escaping 
by  other  channels,  viz.  through  the  lacerated  membranes. 

The  freezing-point  of  the  cerebro -spinal  fluid  has  been  studied 
by  various  observers  : — so-called  cryosco'pic  examination.  Widal, 
Sicard,  Eavaut,^  and  others  have  recorded  a  lowering  of  the 
freezing-point  in  certain  diseases  such  as  meningitis,  tuberculous 
or  otherwise.  But,  on  the  whole,  cryoscopy  has  not  been  of  much 
practical  value. 

(2)  Chemical  Characters. — These  are  of  some  value.  Thus,  for 
example,  a  marked  excess  of  albumin  is  found  in  acute  meningitis, 
and  to  a  lesser  degree  in  tabes  and  in  general  paralysis  of  the  insane, 
the  proteid  concerned  in  tabes  and  general  paralysis  being  an 
euglobulin.  A  convenient  method  of  examining  this  globulin  is  by 
Noguchi's  test,^  which  is  performed  as  follows  :— To  two  parts  of 
cerebro-spinal  fluid  are  added  five  parts  of  a  10  per  cent,  solution 

1  Scot.  Med.  and  Surg.  Journ.,  Edinburgh,  1902,  p.  145. 
*  Compi.  rend.  Soc.  de  Biol,  Paris,  August  20,  1900. 
^  Journal  of  Experimental  Medicine,  1909,  vol.  xi.  p.  84. 


THE    CEREBRO-SPINAL    FLUID  409 

of  butyric  acid  in  normal  saline  solution.  This  mixture  is  heated 
to  boiling-point,  and  then  one  part  of  a  normal  (4  per  cent.)  solution 
of  sodium  hydrate  is  added  and  the  mixture  is  again  boiled  briefly. 
On  standing  for  two  to  thirty  minutes,  if  a  globulin  be  present, 
there  is  a  flocculent  or  granular  precipitate.  An  even  simpler 
method  of  detecting  globulin  (and  one  which  is  free  from 
the  olfactory  drawbacks  of  Noguchi's  method)  is  by  means  of 
ammonium  sulphate.'^  On  to  the  surface  of  a  saturated  solution  of 
ammonium  sulphate  in  a  test-tube  a  small  amount  of  cerebro- 
spinal fluid  is  allowed  to  flow  by  means  of  a  fine  pipette.  If 
globulin  be  present,  a  fine  white  ring  appears  at  the  junction  of 
the  two  fluids. 

In  acute  meningitis,  whether  tuberculous  or  septic,  sugar  is 
almost  always  absent.  In  chronic  meningitis,  in  tabes,  and  in 
general  paralysis  of  the  insane,  it  is  often  diminished. 

Another  chemical  point,  which  my  colleague.  Dr.  Hebb,  in- 
vestigated in  a  number  of  my  cases  at  the  Westminster  Hospital, 
is  as  to  the  presence  of  cholin  in  the  cerebro-spinal  fluid.  Nor- 
mally cholin  is  not  detectable  in  any  appreciable  quantity.  But 
in  organic  degenerative  diseases  of  the  nervous  system,  cholin  may 
be  demonstrated  in  the  blood  and  cerebro-spinal  fluid,  and  can  be 
crystallised  out  as  a  combined  platinum  salt,  according  to  the 
method  of  Halliburton  and  Rosenheim.^  Thus,  for  example,  Hebb 
obtained  cholin-platinum  crystals  from  the  cerebro-spinal  fluid  in 
cases  of  cerebral  hsemorrhage,  syringomyelia,  disseminated  sclerosis, 
&c.  This  test  may  occasionally  be  of  value  in  the  diagnosis  between 
hysteria  and  gross  organic  disease.  But  it  is  too  comphcated  for 
ordinary  clinical  work. 

(3)  Bacteriological  Characters. — These  are  chiefly  of  value  in 
cases  of  meningitis,  to  determine  the  particular  organism  causing 
the  disease.  Thus,  for  example,  in  epidemic  cerebro-spinal 
meningitis  the  meningo-coccus  {diplococcus  intra-cellularis)  is  found  ; 
in  tuberculous  meningitis,  the  tubercle  bacillus  ;  and  in  other 
varieties  of  meningitis  we  may  find  staphylococci,  streptococci, 

1  Jones,  Review  of  Neurol,  and  Psychiatry.  1909,  p.  379. 

2  Brit.  Med.  Journ.,  1907,  p.  1043. 


410  NERVOUS    DISEASES 

pneumococci,  and  so  on.  We  should  remember  that  failure  to 
discover  tubercle  bacilli  does  not  necessarily  exclude  tuberculous 
meningitis,  though  their  presence  would  confirm  such  a  diagnosis. 

To  demonstrate  tlie  bacilli  in  tuberculous  meningitis  it  is  convenient  to 
allow  the  fluid  to  stand  for  12  to  24  hours,  by  which  time  a  fine  coagulum 
has  usually  formed.  This  is  removed  by  a  needle,  spread  on  a  slide,  fixed  and 
stained  in  the  usual  manner. 

In  doubtful  cases  inoculation  experiments  on  guinea-pigs  are  of 
value.  In  Landry's  ascending  paralysis  various  organisms  (tetra- 
cocci  and  others)  have  occasionally  been  isolated  from  the 
cerebro -spinal  fluid  and  blood. 

(4)  Microscopic  Characters. — Clinically,  microscopic  investiga- 
tion has  proved  by  far  the  most  valuable  mode  of  examination 
of  the  cerebro-spinal  fluid.  A  good  method  is  to  centrifuge  a 
given  quantity  of  the  fluid,  say  5  c.c.  for  five  minutes,  thereby 
collecting  into  a  small  deposit  all  the  cellular  elements  which  may 
be  present.  We  then  carefully  decant  off  all  the  superjacent  fluid, 
turn  the  empty  tube  upside  down  and  scrape  the  bottom  with 
a  fine  capillary  pipette.  In  this  way  we  collect  the  sediment, 
which  is  transferred  to  a  slide,  fixed  by  heat,  stained  by  methyl 
blue  or  by  Jenner's  stain,  mounted  in  Canada  balsam  and  examined- 
with  the  microscope. 

Specimens  prepared  as  above  described  afford  a  permanent 
record  of  the  variety  and  intensity  of  the  cellular  contents  present. 
To  obtain  absolute  accuracy  of  counting  we  employ  Fuchs  and 
Rosenthal's  ^  counting-chamber,  a  modification  of  the  Zeiss  blood- 
counting  chamber.  In  using  this,  a  small  quantity  (10  cubic  mm.) 
of  cerebro-spinal  fluid  is  mixed  by  means  of  a  special  pipette  with 
1  cubic  mm.  of  a  staining  fluid  containing  methyl  violet  and 
acetic  acid.  A  drop  of  the  mixture  is  placed  on  the  counting 
stage,  and  the  cells  are  counted.  The  results  so  obtained  corre- 
spond with  those  found  in  centrifuged  deposits,  but  are  more 
accurate.  But  the  preparation  so  obtained  is  not  a  permanent 
one,  and  I  am,  therefore,  now  in  the  habit  of  employing  both  the 
centrifuge  and  the  counting  chamber — the  one  to  yield  a  permanent 

^  Wiener  medizinische  Presse,  1904,  s.  2084. 


THE    CEREBRO-SPINAL    FLUID  411 

specimen,  the  otlier  to  ensure  accurate  counting  of  the  cellular 
contents  in  the  fluid. 

In  rare  cases  we  may  find  parasites.  Thus,  for  example, 
Castellani  and  Bruce  ^  found  the  trypanosome  of  sleeping-sickness 
not  only  in  the  blood  of  such  patients  but  also  in  the  cerebro- 
spinal fluid.  In  fact,  it  is  easier  to  identify  the  trypanosome  in 
the  cerebro-spinal  fluid  than  in  the  blood,  where  it  is  likely  to  be 
obscured  by  blood  corpuscles.  In  a  few  cases  of  malignant  growths 
of  the  spinal  cord  or  of  its  meninges,  tumour-cells  have  been  found 
in  the  fluid.  But  this  is  inconstant,  though  tumour-cells,  if  present, 
would  have  a  high  positive  diagnostic  value. 

By  far  the  most  valuable  point  to  be  determined  microscopicaUy 
is  the  presence  or  otherwise  of  leucocytes,  observing  not  only  their 
number  but  their  type.     This  is  the  so-called  cyto-diagnosis. 

Normal  cerebro-spinal  fluid  contains  no  polymorpho-nuclear 
leucocytes  and  only  an  occasional  small  mono-nucleated  lymphocyte, 
with  now  and  then  a  few  endothelial  plates.  Examination  of  the 
centrifuged  deposit  with  a  magnification  of  400  diameters,  accord- 
ing to  the  technique  described,  should  show  an  average  of  not  more 
than  two  or  three  lymphocytes  to  the  field,  or  from  1  to  2  per 
cubic  mm.  Sometimes  we  find  no  cells  of  any  sort.  But  in 
certain  organic  diseases  of  the  central  nervous  system  or  its  mem- 
branes, there  may  be  a  large  excess  of  leucocytes — ^polymorphs 
or  monomorphs.  Briefly  stated,  in  cases  of  acute  microbic  in- 
fection of  the  brain  and  meninges,  especially  the  suppurative 
varieties,^  we  find  a  polynuclear  leucocytosis,  where  the  leucocytes 
are  mostly  polymorphs,  with  some  large  monomorphs  as  well. 
When  recovery  begins  in  acute  infective  meningitis,  the  poly- 
nuclear leucocytes  in  the  cerebro-spinal  fluid  diminish  in  numbers 
and  become  replaced  by  lymphocytes.  These  latter  in  turn  dis- 
appear as  convalescence  becomes  complete. 

1  Brit.  Med.  Journ.,  November  21,  1903. 

^  But  it  is  the  acuteness  of  the  inflammatory  process,  not  its  microbic 
origin,  which  appears  to  be  the  chief  factor  in  producing  polynuclear  leuco- 
cytosis. Thus  I  have  experimentally  produced  abundant  polynuclear  leuco- 
cytosis in  monkeys  by  injecting  sterile  salt  solution  or  a  sterile  emulsion  of 
coloured  particles  mto  the  spinal  theca. 


412  NERVOUS    DISEASES 

If  a  brain  abscess  be  present  witbout  implication  of  tbe 
superjacent  meninges,  as  sometimes  occurs,  tbe  cerebro-spinal  fluid 
sbows  no  excess  of  leucocytes.  Examination  of  tbe  fluid  is  tbere- 
fore  a  valuable  means  of  distinguisbing  between  meningitis  and 
brain  abscess.  In  botb  conditions  a  blood-count  sbows  a  great 
excess  of  polymorphs  in  tbe  blood  :  tbese  may  number  from 
10,000  to  25,000  or  more  (instead  of  from  8000  to  10,000  per  cubic 
millimetre  as  in  health),  the  leucocytosis  of  the  blood  being  higher, 
as  a  rule,  in  meningitis  than  in  brain  abscess. 

But  in  subacute  and  chronic  afiections  of  the  meninges,  whether 
tuberculous,  syphilitic,  or  otherwise,  also  in  certain  chronic  de- 
generative diseases  of  the  central  nervous  system,  we  usually  find 
a  lymphocytosis,  i.e.  an  excess  of  small  monomorphs,  sometimes 
accompanied  by  a  small  proportion  of  large  monomorphs.  In 
cases  of  acutely  advancing  tuberculous  meningitis  I  have  also 
found  a  considerable  proportion  of  polymorphs  (30  per  cent,  and 
upwards)  amongst  the  monomorphs.  There  is  often  a  marked 
lymphocytosis  during  an  attack  of  herpes  zoster  and  for  a  number 
of  days  afterwards.  In  functional  nervous  diseases  the  fluid  is 
normal. 

In  several  cases  of  lymphatic  leuksemia,  and  in  a  case  of 
chloroma  at  the  Westminster  Hospital,  Hebb  has  also  observed 
marked  lymphocytosis  of  the  cerebro-spinal  fluid. 

Let  us  study  some  illustrative  cases.  One  case  was  an  example 
of  epidemic  cerebro-spinal  meningitis  in  a  patient  who  was  comatose 
and  apparently  moribund.  The  cerebro-spinal  fluid  was  under 
excessive  pressure,  of  turbid  appearance,  and  the  centrifuged 
deposit  showed  microscopically  an  average  of  87'3  polymorphs  to 
the  field.  Within  many  of  the  leucocytes  the  meningo -coccus  was 
readily  distinguished.  The  withdrawal  of  about  an  ounce  of  fluid 
caused  marked  improvement  in  the  symptoms  and  the  patient 
made  a  good  recovery.  Another  case  was  that  of  an  officer  who 
had  chronic  otitis  media  on  the  left  side.  He  rapidly  developed 
mental  dulness  and  slight  aphasic  symptoms,  with  some  fever.  In 
his  case  the  fluid  was  turbid,  and  showed  no  fewer  than  371  poly- 
morphs to  the  field.     Operation  was  at  once  undertaken  and  an 


THE    CEREBRO-SPINAL    ELUE)  413 

inflamed  area  of  brain  tissue  was  exposed  in  the  temporal  lobe. 
No  abscess  was  found.  The  symptoms  rapidly  subsided  and  the 
patient  made  a  complete  recovery. 

As  an  instance  where  the  cerebro-spinal  fluid  was  normal  may 
be  mentioned  the  case  of  a  child,  in  whom,  as  is  so  often  the 
case,  a  deep-seated  pneumonia  was  ushered  in  by  head  symp- 
toms simulating  meningitis — so-called  "  meningism."  There  were 
marked  headache,  some  head-retraction,  and  squint.  Moreover, 
an  older  child  in  the  same  family  had  previously  died  from  menin- 
gitis, and  the  parents  were  therefore  in  considerable  anxiety  as  to 
the  possibility  of  a  second  case.  The  cerebro-spinal  fluid,  however, 
showed  no  excess  of  cells,  and  Kernig's  sign  was  absent.  Meningitis 
was  therefore  less  likely  than  a  functional  meningism,  and  an 
encouraging  prognosis  was  given,  which  proved  correct. 

With  regard  to  the  cases  of  lymphocytosis,  the  most  striking 
results  are  those  observed  in  general  paralysis  of  the  insane  and 
in  tabes  dorsalis.  The  lymphocytosis  in  these  two  afiections 
(which  are  essentially  the  same  disease  etiologically,  and  which 
clinically  are  not  infrequently  combined  in  the  same  patient)  is 
more  marked  than  in  any  other  form  of  organic  nervous  disease. 
Thus  in  a  recent  series  of  twelve  cases  of  general  paralysis  examined 
by  me,  the  average  number  of  lymphocytes  was  131  per  cubic-mm., 
the  lowest  count  in  any  one  case  being  40-5,  and  the  highest  295. 
In  a  series  of  fiiteen  tabetics,  the  lowest  count  was  14,  the  highest 
477' 1,  and  the  average  number  per  cubic  mm.  for  the  whole  series 
was  125'4.  This  closely  approximates  to  the  average  for  general 
paralysis. 

A  point  of  importance  noticed  in  cases  of  tabes  and  general 
paralysis  is  that  not  only  is  lymphocytosis  present  in  practically 
every  case,  but  it  is  often  extremely  marked  when  the  other 
symptoms  of  the  disease  are  very  slight.  Thus,  for  example,  one 
patient  had  lightning-pains,  analgesia  of  the  tendo  Achillis,  but  no 
ataxia,  no  abnormality  of  the  pupils,  and  brisk  knee-  and  ankle- 
jerks.  Yet  his  cerebro-spinal  fluid  showed  150  lymphocytes  per  cubic 
millimetre,  and  he  was  undoubtedly  an  early  case  of  tabes.  The 
same  applies  to  general  paralysis.     One  patient  with  239'6  lympho- 


414  NERVOUS    DISEASES 

cytes  per  cubic  mm.  was  an  early  case,  witli  practically  no  mental 
symptoms,  simply  a  slight  loss  of  memory  and  a  history  of  two 
attacks  of  unconsciousness  followed  by  transient  aphasia  and 
weakness  of  the  right  hand — "  congestive  attacks." 

We  therefore  possess  in  the  cytological  examination  of  the 
cerebro -spinal  fluid  a  valuable  means  of  recognising  tabes  and 
general  paralysis  in  their  earliest  stages .  If  no  excess  of  lymphocytes 
is  present,  these  two  diseases  can  usually  be  excluded.^  Another 
point  of  interest  is  that  during  the  pyrexial  attacks  of  general 
paralysis,  there  is  a  temporary  polynuclear  leucocytosis  not  only 
of  the  blood  but  of  the  cerebro-spinal  fluid.  Thus  in  a  case  of 
my  own  there  were  118  polymorphs  and  25  monomorphs  per  cubic 
mm.     Pappenheim  ^  has  also  recorded  similar  cases. 

A  further  point  of  interest  is  that  the  lymphocytosis  in  tabes 
and  general  paralysis  is  uninfluenced  by  the  most  energetic  anti- 
specific  treatment.  In  several  of  my  cases,  the  fluid  was  examined 
at  intervals  of  a  month,  the  patient  meantime  having  had 
daily  hypodermic  administrations  of  mercury ;  yet  the  lympho- 
cytosis remained  unchanged  in  its  intensity.  This  is  in  marked 
contrast  to  what  occurs  in  active  syphilitic  lesions.  Thus,  for 
example,  in  a  case  of  gumma  of  the  spinal  cord,  the  lymphocytes, 
which  numbered  52 "6  on  admission,  were  reduced  after  three 
weeks'  treatment  to  16' 1,  and  the  patient,  who  was  totally  para- 
plegic and  anaesthetic  in  the  lower  hmbs  on  admission,  was 
discharged  in  a  couple  of  months  able  to  walk,  without  anaesthesia, 
and  with  the  sphincters  under  control. 

Another  point  of  importance  is  that  syphilis  by  itself,  unless 
there  be  an  active  syphihtic  lesion  of  the  central  nervous  system, 
produces  httle  or  no  excess  of  lymphocytes  in  the  cerebro-spinal 
fluid.  Thus  in  my  series  of  twelve  cases,  in  the  five  secondary 
cases    the   average    number    of    lymphocytes  was    2*7,    that    of 

^  This  rule,  however,  is  not  without  exceptions,  for  I  have  seen  a  case  of 
tabes,  with  ataxia,  Argyll-Robertson  pupils,  and  absent  knee-  and  ankle-jerks, 
in  which  the  cerebro-spinal  fluid  contained  only  3-3  lymphocytes  per  mm'. 
Erb  {Deutsche  Zeitsch.  f.  Nervenheilkunde,  1907,  s.  438)  has  also  recorded 
similar  cases. 

*  Monatschrift  fiir  Psychiatrie  und  Neurologie,  1907,  s.  536. 


THE    CEREBRO-SPINAL    FLUID  415 

tlie  six  tertiary  cases  was  0"9,  the  twelfth  case  being  one  of 
a  man  who  had  a  syphihtic  chancre  twenty-six  years  before. 
The  tertiary  cases  with  active  syphihtic  lesions,  such  as  gum- 
matous ulcers,  rupia,  and  so  on,  had  more  cells  than  the  others, 
but  even  in  them  the  number  was  less  than  the  average  of  the 
secondary  cases. 

We  thus  see  that  the  presence  of  a  large  lymphocytosis  in  a 
patient  who  has  had  syphihs,  is  of  grave  significance  and  indicates 
serious  organic  disease,  either  a  syphilitic  lesion  of  the  central 
nervous  system,  or,  if  very  marked,  tabes  or  general  paralysis. 
In  such  cases  we  should  carefully  examine  for  other  signs  of  organic 
disease,  especially  for  Argyll-Robertson  pupils,  early  optic  atrophy, 
alterations  in  the  reflexes,  and  sensory  changes.  Even  if  no 
other  sign  of  organic  disease  be  present,  the  presence  of  lympho- 
cytosis of  the  cerebro- spinal  fluid  is  an  indication  for  the  most 
energetic  anti-specific  treatment,  in  the  hope,  perhaps,  of  preventing 
subsequent  developments. 

The  presence  of  lymphocytosis  in  tuberculous  meningitis  is 
readily  understood,  also  that  which  occurs  in  tuberculous  tumours 
on  the  surface  of  the  brain.  It  is  more  difficult  at  present  to 
account  for  the  occasional  excess  of  lymphocytes  in  cerebral 
neoplasms.  Thus  one  case  of  glioma  of  the  centrum  ovale  had  no 
fewer  than  75  lymphocytes  to  the  field,  a  count  which  led  one 
to  expect  a  tuberculous  mass,  there  being  no  possibihty  of  syphilis. 
Yet  the  autopsy  showed  a  glioma  which  had  in  no  way 
approached  the  meninges,  and  where  a  haemorrhage  into  the 
substance  of  the  tumour  ultimately  caused  death  by  bursting 
into  the  lateral  ventricle. 

Therapeutic  Applications  of  Thecal  Puncture. — ^Lumbar 
puncture  was  originally  introduced  by  Quincke  for  the  purpose 
of  relieving  intra -cranial  pressure  in  tuberculous  meningitis.  This 
it  does  for  the  time,  though  it  is  more  often  palliative  than  curative. 
In  one  case  of  mine  the  patient,  a  young  man,  comatose  and 
apparently  moribund,  regained  consciousness  for  a  day,  after  the 
withdrawal  of  22  c.c.  of  cerebro -spinal  fluid.  The  fluid  was  allowed 
to  flow  until  the  increased  intra-thecal  pressure  fell  to  normal. 


416  NERVOUS    DISEASES 

The  importance  of  this  procedure,  not  only  from  sentimental 
reasons  but  possibly  on  medico -legal  grounds,-  is  obvious.  In 
any  case  we  can  usually  diminish  or  abolish  the  convulsions 
which  are  so  distressing  to  the  onlookers.  But  sometimes 
lumbar  puncture  has  undoubtedly  proved  curative,  even  in 
tuberculous  meningitis.  Thus  in  cases  recorded  by  Freyhan,^ 
Henkel,^  Barth,^  and  others,  tubercle  bacilli  were  demonstrated 
in  the  cerebro -spinal  fluid  and  yet  the  patients  ultimately  recovered, 
after  repeated  punctures. 

In  other  forms  of  meningitis  associated  with  a  polynuclear 
leucocytosis  (apart  from  infective  cases  secondary  to  bone  disease), 
especially  in  epidemic  cerebro -spinal  meningitis,  good  results  have 
been  obtained  by  the  injection  of  antiseptic  substances,  after  with- 
drawal of  a  corresponding  quantity  of  cerebro -spinal  fluid.  For 
this  purpose,  a  1  per  cent,  solution  of  lysol  has  been  found  useful, 
10  cubic  centimetres  being  introduced  at  each  sitting.  Flexner's 
serum,  prepared  from  immunised  horses,  injected  in  doses  of 
about  30  c.c.  repeated  on  several  successive  days,  has  also  had 
highly  encouraging  results.* 

In  intra-cranial  pressure  due  to  other  causes,  as,  for  example, 
in  inoperable  or  inaccessible  cerebral  tumours,  lumbar  puncture  is 
sometimes  of  distinct  benefit  as  a  palliative  measure,  by  diminishing 
urgent  pressure  and  theireby  relieving  headache,  vertigo,  and  other 
symptoms.  Hitherto  to  relieve  intra-cranial  pressure  and  to 
diminish  optic  neuritis  it  has  been  the  custom,  to  trephine  the 
skull  as  a  palliative  measure.  But  lumbar  puncture  is  quicker, 
simpler,  and  less  dangerous  than  a  major  cranial  operation.  I  per- 
formed it  in  three  cases  of  intra-cranial  tumour  where  the  symptoms 
pointed  to  deep-seated  cerebellar  disease.  In  all  of  them  the 
headache  and  vertigo  were  greatly  relieved  for  several  weeks  after 
the  puncture,  and  an  opportunity  was  afforded  of  studying  the 
patient's  focal  symptoms  with  a  view  to  subsequent  removal  of  the 
growth.       In  intra-cranial  growths  we   must  be   careful  not  to 

^  Deutsche  medizinische  Wochenschrift,  1904,  No.  36. 
^  Munchener  medizinische  Wochenschrift,  1900,  s.  133. 
3  Ibid.,  1902,  No.  21. 
^  Ker,  Edin.  Med.  Journal,  Oct.  1908. 


THE    CEREBRO-SPINAL    FLUID  417 

withdraw  too  large  a  quantity  of  cerebro-spinal  fluid,  lest  sudden 
diminution  of  pressure  cause  a  hsemorrhage  into  the  tumour  (a 
result,  by  the  way,  which  sometimes  occurs  after  a  palliative 
trephining).  In  a  case  recorded  by  Masing  ^  this  actually  occurred  ; 
but  in  his  case  the  fluid  was  allowed  to  run  for  a  quarter  of  an  hour 
and  no  less  than  10  c.c.  were  withdrawn.  I  have  had  under  my 
observation  several  cases  of  persistent  tinnitus  and  giddiness,  of 
many  months'  duration,  in  which  a  single  lumbar  puncture  with 
the  removal  of  less  than  10  c.c.  of  fluid  permanently  relieved  the 
condition.  We  must,  of  course,  be  careful  to  eUminate  all  the 
ordinary  causes  of  tinnitus  and  giddiness,  aural  or  otherwise,  before 
resorting  to  this  treatment.  In  fractures  of  the  base  of  the  skull, 
coma  may  be  relieved  in  a  remarkably  short  time  by  the  with- 
drawal of  cerebro-spinal  fluid.  I  saw  such  a  patient  after  a 
carriage  accident,  in  whom  lumbar  puncture  was  followed  by 
rapid  improvement.  The  procedure  may,  if  necessary,  be  repeated 
several  times  on  successive  days. 

Ursemic  coma  and  convulsions,  and  cases  of  puerperal  eclampsia, 
are  often  relieved  in  a  striking  manner  by  lumbar  puncture,  and  in 
several  instances  life  has  undoubtedly  been  saved  by  this  means. 
For  example,  McVail  ^  records  two  cases  of  acute  nephritis  in  which, 
notwithstanding  energetic  treatment  by  purgatives,  hot-air  baths 
and  pilocarpin  to  induce  free  perspiration,  coma  and  convulsions 
supervened.  Lumbar  puncture  was  performed,  20  to  28  c.c.  of 
cerebro-spinal  fluid  were  withdrawn,  and  within  three  or  four 
hours  the  coma  passed  off,  the  convulsions  ceased,  and  both  patients 
ultimately  made  a  complete  recovery.  Cases  like  these  raise  the 
question  as  to  whether  the  headache,  coma,  and  convulsions  in 
nephritis  are  really  caused  entirely  by  "  ursemic  poisoning  "  of  the 
brain-centres,  or  whether  they  may  not  be  largely  due  to  a  sudden 
increase  of  intra-cranial  pressure — part  of  the  general  oedema. 

Again,  in  cases  of  tetanus,  we  know  that  the  tetanus  poison 
has  a  selective  action  on  the  motor  nerve-cells  of  the  spinal  cord 
and    brain.      Therefore,    in    addition    to    removing    the    tetanus 

1  Neurol.  Centralbl,  1904,  p.  1116. 

2  Brit.  Med.  Journ.,  1903,  vol.  ii. 

2d 


418  NERVOUS    DISEASES 

bacilli  at  the  site  of  inoculation,  by  excision  of  the  original  M^ound, 
we  endeavour  to  neutraHse  the  toxin  by  means  of  antitoxin. 
This  is  sometimes  administered  hypodermically ;  but  it  is  more 
efficacious,  as  Eoux  and  others  have  shown,  if  injected  into 
the  cranial  cavity  through  a  small  trephine  opening,  and  some 
remarkable  recoveries  have  followed  this  method  of  treatment. 
But  the  procedure  is  not  free  from  danger.  In  one  case  at  least, ^ 
a  patient  died  of  cerebral  abscess  at  the  site  of  the  trephine - 
opening  eight  weeks  afterwards,  long  after  all  symptoms  of  tetanus 
had  disappeared.  It  is  simpler  and  better  to  administer  the  anti- 
toxin (with  perhaps  the  addition  of  stovaine  and  morphine)  by 
means  of  a  lumbar  puncture  needle.  Strychnine  poisoning  is  also 
successfully  treated  by  intra-thecal  administration  of  eucaine.  It 
may  be  necessary  to  give  a  general  anaesthetic  to  relax  the 
opisthotonos,  before  performing  the  spinal  puncture. 

Injection  of  anaesthetic  drugs  by  thecal  puncture — so-called 
spinal  anaesthesia — is  useful  when  we  desire  to  perform  operations 
on  the  lower  limbs  or  trunk  without  rendering  the  patient's  brain 
unconscious.  Various  substances  have  been  successfully  employed 
as  spinal  anaesthetics,  amongst  which  may  be  mentioned  cocaine, 
stovaine,  and  a  mixture  of  novocaine  with  strychnine.^  It  is 
desirable,  if  possible,  to  have  a  solution  which  is  isotonic  with 
the  blood-serum,  i.e.  having  the  same  osmotic  tension. 

Eor  spinal  anaesthesia  in  operations  on  the  pelvis  and  lower 

1  Gibbs,  Brit.  Med.  Journ.,  July  1,  1899. 

2  The  following  are  examples  of  arsesthetising  solutions : — 

1.  Stovaine,  5  per  cent.;  glucose,  5  per  cent,  in  water.  Sp.  gr.  =  1023. 
Dose  =  l  c.c.     (Barker,  Brit.  Med.  Journ.,  1908,  p.  248.) 

2.  Stovaine,  4  per  cent.;  sod.  chloride,  0"11  per  cent.  ;  suprarenin 
borate,  0"01  per  cent,  in  water.  Sp.  gr.  =  1005.  Dose  =  l  c.c.  (Bier, 
quoted  by  Barker,  Brit.  Med.  Journ.,  1907,  p.  665.) 

3.  Stovaine,  1 '5  per  cent. ;  cocaine,  0*5  per  cent,  in  water.  Doss  =  4  c.c. 
(Chaput,  La  Presse  Medicale,  1907,  p.  753.) 

4.  Novocaine,  2  per  cent. ;  suprarenin  borate,  0*009  per  cent. ;  NaCl, 
0'9  per  cent.  Sp.  gr.  =  1014.  Dose  =  5  c.c.  (Braun,  Deutsche  med. 
Wochenschrift,  1905,  s.  1667.) 

5.  Strychnine  sulphate,  5  to  10  eg. ;  sterilised  water,  100  grams.  Of 
this  solution  1  c.c.  is  mixed  with  3  to  10  eg.  of  stovaine,  and 
the  mixture  is  injected.  (Jonnesco,  Brit.  Med.  Journal,  1909, 
p.  1396.) 


THE    CEREBRO-SPINAL    FLUID  419 

limbs  we  generally  select  the  fii'st  or  second  lumbar  interspace, 
whilst  Jonnesco  prefers  "  dorso-lumbar "  injection  between  the 
twelfth  thoracic  and  the  first  lumbar  vertebra,  thereby  producing 
analgesia  of  the  whole  abdomen  and  lower  limbs.  We  perform 
our  puncture  in  the  mesial  line,  so  that  the  roots  of  both  sides 
may  be  equally  afiected.  Before  injecting  the  ansesthetising 
solution,  we  withdraw  a  quantity  of  cerebro-spmal  fluid,  ex- 
ceeding in  amount  the  fluid  to  be  introduced. 

Spinal  ansesthesia  is  essentially  a  root  anaesthesia,  due  to 
paralysis  of  the  posterior  roots.  On  injecting  a  solution  of 
stovaine  m  the  lumbar  region,  the  earliest  objective  signs  are 
disappearance  of  the  knee-jerks  (usually  within  one  minute),  then 
of  the  ankle -jerks  (within  two  or  three  minutes),  the  superficial 
reflexes  remaining  as  yet  unchanged.  Concurrently  with  the 
abolition  of  the  deep  reflexes  there  occurs  slight  analgesia  of  the 
perineum  and  genitals,  without  loss  of  tactile  sensibility.  The 
analgesia  gradually  deepens  and  spreads  over  the  lower  limbs,  and 
after  four  or  five  minutes  the  plantar  and  cremasteric  reflexes 
disappear.  Temperature -sense  becomes  lost.  Tactile  and  pressure- 
sense  disappear  much  later  and  may  be  preserved  throughout. 
Sense  of  position  is  last  and  least  affected.  The  dartos  or  scrotal 
reflex  is  unaffected.  Motor  paralysis,  due  to  affection  of  the 
anterior  roots,  supervenes  last  of  all,  in  five  or  six  minutes, 
beginning  in  the  feet  and  soon  affecting  the  whole  musculature  of 
the  lovter  limbs.  The  deep  structures  also  become  analgesic.  If  it 
is  desired  to  reach  the  higher  roots  by  a  heavy  ansesthetising  fluid, 
it  is  advisable  to  elevate  the  pelvis  higher  than  the  thorax,  to 
permit  the  fluid  to  gravitate  towards  the  thoracic  region.  In  this 
way  the  ansesthesia  may  extend  as  high  as  the  nipples,  or  even  to 
the  upper  limbs.  If  the  injection  be  made  with  the  patient  lying 
on  his  side,  the  heavy  ansesthetising  solution  gravitates  to  the 
dependent  side  and  therefore  exercises  its  effects  chiefly,  and  it 
may  be  entirely,  on  the  roots  of  that  side.  Thus,  for  example, 
by  laying  a  patient  on  his  left  side  and  injecting  in  that  posture 
Barker  ^  was  able  to  amputate   the  left  leg  painlessly,  without 

1  Brit.  Med.  Journ.,  1908,  p.  246. 


420  NERVOUS    DISEASES 

producing  sensory  or  motor  impairment  of  the  right  lower 
limb. 

After  lasting  for  45  to  90  minutes,  the  paralytic  phenomena 
begin  to  pass  off.  First  motor  power  returns,  then  the  analgesia 
fades  away,  and  last  of  all,  the  reflexes,  superficial  and  deep, 
reappear. 

Spinal  anaesthesia  by  means  of  stovaine  can  also  be  employed, 
as  Jonnesco  ^  has  shown,  at  higher  levels  of  the  cord  if  strychnine 
be  added  to  the  stovaine  so  as  to  protect  the  cord  from  depressing 
vaso-motor  or  respiratory  effects.  For  operations  on  the  head, 
neck,  and  upper  limbs  Jonnesco  recommends  an  "  upper  dorsal " 
puncture,  between  the  first  and  second  dorsal  vertebrae.  Injections 
at  any  higher  level  are  unnecessary,  besides  being  too  close  to  the 
medulla  oblongata  for  safety.  For  operations  on  the  abdomen 
and  lower  limbs,  Jonnesco  recommends  a  "  dorso-lumbar  "  injection 
between  the  twelfth  dorsal  and  first  lumbar  vertebrae  (see  Fig.  222). 
It  should  be  borne  in  mind  that  both  in  "  upper  dorsal "  and  in 
"  dorso-lumbar  "  punctures  the  spinal  cord  lies  immediately  sub- 
jacent to  the  site  of  the  puncture,  and  it  is  therefore  important 
to  stop  the  needle  immediately  its  point  has  penetrated  within  the 
spinal  theca,  so  as  to  avoid  injury  to  the  spinal  cord. 

In  performing  an  "  upper  dorsal "  injection  we  first  feel  for 
the  vertebra  prominens  (seventh  cervical).  Then  taking  the  first 
dorsal  spine  immediately  below  this  (the  patient's  head  being 
strongly  flexed,  so  as  to  separate  the  laminae),  we  slowly  push  in 
our  needle,  in  the  mesial  plane,  along  the  .upper  border  of  the 
second  dorsal  spine.  On  reaching  the  dura  mater  a  momentary 
resistance  is  felt,  and  when  the  needle  reaches  the  arachnoidal 
space,  cerebro-spinal  fluid  at  once  begins  to  trickle.  Unless  fluid 
is  seen  to  escape,  we  cannot  be  sure  that  the  point  of  the  needle 
is  in  the  arachnoidal  cavity.  Sometimes  it  is  useful  to  make  the 
patient  cough,  to  start  the  fluid.  As  soon  as  the  fluid  begins  to 
escape  we  attach  our  injection-syringe  and  slowly  mtroduce  the 
mixture  of  stovaine  and  strychnine.  After  an  upper  dorsal  injection, 
if  the  operation  is  to  be  on  the  head  or  neck,  the  patient  should 
1  Brit.  Med.  Journ.,  1909,  p.  1398. 


THE    CEREBRO-SPINAL    FLUID 


421 


be  on  his  back.     If  the  operation  is  to  be  on  the  upper  limbs  or 

thorax,  he  should  sit  up  for  two  or  three  minutes  before  lying  down. 

For  upper  dorsal  injections  Jonnesco   recommends  relatively 

smaller  amounts  of  strychnine  (|  mg.)  and  of  stovaine  (1  to  3  eg.), 


2  D. 


Fig.    222. — Showing  sites  of  "  upper  dorsal  "  and  of  "  dorso-lumbar  " 
injections  for  spinal  ansesthesia.     (Jonnesco.) 

whereas  in  dorso-lumbar  injections  the  doses  of  strychnine  (1  mg.) 
and  of  stovaine  (4  to.  10  eg.)  are  large. 

Spinal  anaesthesia  is  contra -indicated  in  severe  scoliosis,  because 
of  the  difficulty  in  accurately  penetrating  the  theca.  It  is  also 
better  avoided  in  young  children  and  in  most  cases  of  hysteria. 
Even  apart  from  such  cases,  it  should,  I  believe,  be  reserved  for 
very  special  conditions,  as,  for  example,  acute  abdominal  cases, 
conditions  of  shock,  and  severe  cardiac  or  pulmonary  diseases 
where  a  general  anaesthetic  is  particularly  dangerous.  From  the 
patient's  point  of  view,  complete  unconsciousness  is  generally 
preferable  to  the  mental  strain  of  remaining  conscious  whilst  an 
operation  is  being  performed  on  his  analgesic  legs  or  trunk. 


422  NEKVOUS    DISEASES 

Of  the  morbid  phenomena  which  sometimes  follow  spinal 
anaesthesia,  the  most  frequent  is  headache  ;  this  is  often  of  great 
severity  and  may  last  for  days  ;  it  is  probably  due  to  the  altered 
intra -cranial  pressure  produced  by  the  addition  of  the  angesthetising 
solution,  and  may  generally  be  relieved  by  a  simple  lumbar  pimcture, 
withdrawing  from  10  to  20  c.c.  of  fluid.  In  three -fourths  of  cases 
of  spinal  anaesthesia,  according  to  Schwarz,^  there  is  a  slight  transient 
albuminuria,  lasting  for  a  week  or  more.  Another  sequela,  fortu- 
nately an  uncommon  one,  is  ocular  palsy,  chiefly  of  one  external 
rectus  but  sometimes  of  some  other  ocular  muscle  ;  such  palsy 
may  last  for  days  or  weeks,  but  ultimately  clears  up. 

^  Zeitschrift  fur  Chirurgie,  1907,  s.  651. 


CHAPTER   XXIV 

DISORDERS    OF    SLEEP 

•'  The  innocent  sleep, 
Sleep  that  knits  up  the  ravelled  sleave  of  care, 
The  death  of  each  day's  life,  sore  labour's  bath, 
Balm  of  hurt  minds,  great  nature's  second  course, 
Chief  nourisher  in  life's  feast." 

— Shaxespeaee,  Macbeth. 

Most  of  us  spend  about  one-third  of  our  life  asleep.  Neverthe- 
less the  physiology  of  sleep  is  not  yet  completely  understood.  Let 
us  recall  the  chief  phenomena  of  ordinary  healthy  sleep.  Firstly, 
there  is  diminution  and  then  loss  of  conscious  recognition  of  ordi- 
nary stimuli,  such  as  would  ordinarily  attract  our  attention, 
whether  these  stimuli  be  derived  from  the  outer  world  or  from 
within  the  sleeper's  own  organism.  There  is  also,  as  consciousness 
is  becoming  blunted,  a  characteristic  and  indescribable  sense  of 
well-being.  Voluntary  movements  become  languid  and  ultimately 
cease,  and  the  muscles  of  the  limbs  relax.  Meanwhile  there 
develops  double  ptosis  or  drooping  of  the  eyelids  ;  the  pupils  con- 
tract ;  the  respiratory  movements  become  slower  and  deeper,  the 
pulse  is  slowed,  the  cutaneous  vessels  dilate  to  a  slight  extent  and 
the  general  temperature  of  the  body  falls,  whilst  many  processes  of 
metabolism,  such  as  those  of  digestion  and  of  certain  secretions, 
are  retarded. 

Various  explanations  have  been  offered  to  account  for  all  these 
phenomena.  But  at  the  outset  we  should  recognise  that  the 
process  is  a  complex  one,  implicating  many  other  organs  besides 
the  brain.  An  animal  from  which  the  cerebral  hemispheres  have 
been  removed  still  shows  regular  alternations  of  sleep  and  waking. 

As  regards  the  condition  of  the  brain  during  natural  sleep,  it 
is  generally  admitted  that  it  is  ansemic.  If  we  observe  a  patient 
or  an  animal  that  has  been  trephined,  we  see  that  during  sleep 


424  NEEVOUS    DISEASES 

the  volume  of  the  brain  is  diminished  ;  it  sinks  in  and  becomes 
pale,  i.e.  the  cortical  vessels  are  contracted.  This  vaso-con- 
striction  is  not  confined  to  the  superficial  vessels  alone  ;  it  implicates 
the  whole  cerebral  circulation,  for  if  we  succeed  in  examining  the 
patient's  retinal  vessels  with  an  ophthalmoscope  without  wakening 
him,  we  find  that  they  present  a  similar  vaso-constriction.  Cerebral 
anaemia,  then,  is  one  important  factor  in  natural  sleep.  After  a 
heavy  meal  we  are  all  familiar  with  the  difficulty  of  doing  mental 
work  and  the  tendency  to  fall  asleep.  This  is  doubtless  explained 
to  some  extent  by  the  occurrence  of  temporary  abdominal  hyper- 
semia  together  with  compensatory  cerebral  anaemia. 

Let  us  next  consider  the  condition  of  the  nerve -cells  during 
sleep.  The  activity  of  some  of  them,  certamly  of  the  cortical 
cells,  is  temporarily  diminished.  Some  writers  have  suggested 
that  this  is  due  to  a  retraction  of  the  dendrites,  by  a  sort  of  amoeboid 
movement  whereby  nerve-cells  previously  in  contact  become,  as  it 
were,  temporarily  insulated.  But  the  evidence  in  support  of  this 
theory  is  far  from  convincing.  In  fact,  modern  histological  obser- 
vation goes  to  show  that  nerve-cells  are  not  merely  in  contact 
but  that  neuro-fibrillee  are  continuous  from  cell  to  cell  throughout 
the  nervous  system. 

Other  writers  ascribe  the  phenomena  of  sleep  to  poisoning 
of  the  nerve-cells  by  accumulation  of  CO2,  or  to  intoxication  by 
other  waste -products  of  metabolism  acting  as  narcotics.  Be  this 
as  it  may,  we  must  bear  in  mind,  as  Claparede  -^  has  urged,  that 
neither  CO2  poisoning  nor  intoxication  is  a  necessary  antecedent 
to  sleep.  On  the  contrary,  we  usually  sleep  for  the  purpose  of 
avoiding  auto -intoxication  and  of  preventing  exhaustion,  not 
because  auto -intoxication  or  exhaustion  has  supervened.  Healthy 
sleep  is  not  necessarily  a  poisoning  of  certain  nerve-centres  by 
toxic  by-products.  We  may  feel  intensely  fatigued  without  being 
drowsy  and,  conversely,  we  may  feel  drowsy  without  being 
physically  or  mentally  fatigued.  Moreover  there  is  a  regular 
periodicity  whereby  a  healthy  person,  whether  fatigued  or  not, 
has    a   recurrent   appetite    for  sleep.      Sleep  has  a  constructive, 

^  Archives  de  Biologie,  1905. 


DISORDERS    OF    SLEEP  425 

anabolic,  invigorating  effect  on  the  whole  body.  Part  of  this 
effect  is  doubtless  due  to  physical  rest,  part  perhaps  to  inter- 
ruption in  the  production  of  toxins  arising  from  muscular  con- 
traction, and  part  to  the  absence  of  stimuli  which  during  waking 
hours  excite  nervous  katabolism. 

Some  writers  have  assigned  special  importance  to  a  particular 
region  of  the  brain  in  connection  with  the  function  of  sleep,  and 
especially  to  the  floor  of  the  third  ventricle  and  the  Sylvian  aque- 
duct. In  support  of  this  they  point  out  the  familiar  ptosis  and 
the  tendency  to  divergent  strabismus,  both  of  which  might  be 
explained  as  due  to  paresis  of  the  ocular  nuclei.  They  also  recall 
the  well-established  fact  that  tumours  in  this  region  of  the  brain 
are  specially  likely  to  have  as  an  early  symptom  persistent 
drowsiness.  But  some  of  these  phenomena  can  also  be  explained 
as  due  to  cerebral  anaemia,  the  tumour  at  the  base  mechanically 
compressing  and  narrowing  the  arteries  which  form  the  circle 
of  Willis.  This  has  been  demonstrated  in  several  instances, 
notably  in  a  case  of  tumour  of  the  infundibulum  and  floor  of 
the  third  ventricle  recorded  by  Franceschi.^  I  myself  had 
under  my  care  a  similar  case  in  a  young  woman,  aged  twenty-six, 
with  a  large  cystic  growth  of  the  pituitary  body  and  floor  of  the 
third  ventricle,  in  whom  the  chief  S5miptoms  were  paroxysms  of 
overpowering  sleep.  She  ultimately  passed  into  a  stuporose  con- 
dition and  died.  No  paralytic  phenomena  occurred  during  life, 
nor  was  there  any  optic  neuritis.^  Another  case  was  that  of  a 
young  man  of  thirty-four  who  had  intense  drowsiness,  paroxysmal 
headaches,  and  total  loss  of  sexual  power.  He  also  had  blindness 
of  the  right  eye  and  temporal  hemianopia  of  the  left,  with  slight 
pallor  of  the  right  optic  disc,  signs  pathognomonic  of  a  lesion  of 
the  optic  chiasma.  All  these  phenomena  were  due  to  a  tumour  of 
the  pituitary  body.  His  drowsiness  was  so  intense  that  he  fell 
asleep  if  he  sat  down  and  only  with  difficulty  could  he  be  roused 
for  examination. 

Another  factor  in  the  production  of  natural  sleep  is  the  absence 

^  Rivista  di  patologia  nervosa  e  meniak,  1904,  p.  457. 
2  Review  of  Neurology  and  Psychiatry,  1909,  p.  225. 


426  NERVOUS    DISEASES 

of  violent  external  stimuli  such  as  loud  sounds  or  dazzling  light ; 
therefore  silence  and  darkness,  by  withdrawal  of  stimuli,  conduce 
to  sleep.  The  pleasing  monotony  of  gently  reiterated  stimuli  often 
has  a  similar  soothing  effect  which  is  quite  sui  generis  and 
is  closely  analogous  to  the  condition  of  hypnosis.  It  cannot  be 
ascribed  to  cerebral  ansemia,  to  exhaustion,  nor  to  any  toxic 
action. 

We  recognise  different  degrees  of  normal  sleep,  according  to 
the  strength  of  stimulus  necessary  to  rouse  the  sleeper  to  a  con- 
sciousness of  his  surroundings.  The  lightest  is  that  of  mere 
drowsiness,  a  stage  in  which  the  sleeper,  though  not  directing 
his  conscious  attention  to  surrounding  objects,  can  still  be  easily 
wakened  by  moderate  stimuli  such  as  ordinary  conversation,  light 
touches,  &c.  A  deeper  stage  is  sleep  with  dreams,  where  the 
sleeper  is  unconscious  of  his  surroundings  but  yet  his  psychical 
centres,  uncontrolled  and  deprived  of  the  faculty  of  comparison 
with  his  environment,  produce  a  series  of  fantastic  mental  pictures. 
Under  the  influence  of  dreams  a  sleeper  may,  if  his  cortical  motor 
centres  are  still  active  whilst  the  psycho-sensory  centres  are  un- 
controlled, perform  motor  actions,  as  in  the  well-known  stage  of 
sleep  with  sonmambulism.  But  somnambulism  is  rare  in  health, 
because  ordinarily  the  cortical  motor  centres  are  dulled  simul- 
taneously with  the  sensory.  Still  more  profound  is  the  stage  of 
deep  dreamless  sleep.  This  variety  merges  into  what  under 
pathological  conditions  we  call  stupor  and  ultimately  coma. 
The  chief  distinguishing  point  between  deep  sleep  and  coma  is 
that  a  sleeping  person  can  be  roused  whereas  a  comatose  patient 
cannot. 

Disorders  of  Sleep. — We  sometimes  meet  with  pathological 
drowsiness  or  hypersomnia,  which  is  most  frequently  associated 
with  some  variety  of  toxaemia.  Perhaps  the  most  common 
instance  is  that  of  an  anaemic  young  woman.  Here  the 
drowsiness  may  be  partly  toxic,  due  to  absorption  of  poisons, 
whether  from  a  loaded  intestine,  from  decaying  teeth,  or 
from  other  sources,  but  the  main  element  in  causation  is 
probably   vascular.      In    such    a    case    the    heart   is   devoid  of 


DISORDERS    OF    SLEEP  427 

energy,  and  the  vessels  throughout  the  body  are  flabby  and 
deficient  in  tone.  Therefore  in  the  erect  attitude  the  vessels  of  the 
brain  are  badly  filled,  and  if  the  patient  sits  down  during  the  day 
she  feels  drowsy.  But  when  she  lies  down  at  night,  the  brain  now 
becomes  hypersemic  from  want  of  vascular  tone,  and  the  result  is 
that  she  lies  awake.  This  combination  of  diurnal  drowsiness  with 
nocturnal  wakefulness  is  highly  characteristic.  In  treating  the 
condition,  besides  attacking  the  angemia,  we  often  administer, 
digitalis,  since,  besides  being  a  cardiac  tonic,  it  has  also  a  well- 
marked  vaso -constrictor  action.  If  digitalis  be  combined  with 
iron  and  with  bromide  of  potassium,  the  condition  generally 
rapidly  improves. 

Drowsiness  also  occurs  in  other  conditions.  Myxcedematous 
patients  are  habitually  sleepy  and  stupid,  probably  from  toxsemia 
and  thyroid  insufficiency.  So  also  are  many  idiots  and 
cretins.  After  a  severe  fit  of  epilepsy  it  is  common  for  the 
patient  to  fall  into  a  deep  post-epileptic  sleep,  largely  due, 
no  doubt,  to  toxic  products  produced  by  the  nervous  and  mus- 
cular systems  during  the  fit.  Certain  tumours  of  the  brain,  especi- 
ally those  in  the  region  of  the  floor  of  the  third  ventricle,  as  we 
have  abeady  seen  (p.  425),  are  associated  with  early  and  persistent 
drowsiness  ;  so  also  are  some  cases  of  punctured  wounds  in  the 
same  region.-^  Elsewhere  in  the  brain,  tumours  may  also  produce 
drowsiness  at  a  late  stage  of  the  disease,  probably  from  increased 
intra-cranial  pressure,  though  in  these  cases  the  condition  more 
nearly  approaches  coma  and  ultimately  merges  into  it.  The 
intense  drowsiness  produced  by  the  combination  of  exhaustion 
with  extreme  cold,  as  in  arctic  travellers  or  alpine  climbers 
who  are  in  danger  of  being  frozen  to  death,  is  probably 
largely  due  to  deficient  circulation,  and  unless  vigorous  meas- 
ures be  taken  to  stimulate  the  heart  and  the  general  circula- 
tion, sleep  passes  on  to  coma  and  death.  The  hibernation-sleep 
of  certain  animals  is  largely  due  to  winter-cold,  for  if  such 
animals  be  kept  in  a  warm  atmosphere  throughout  the  winter, 
they  do  not  sleep  more  than  in  summer  time.  The  delightful 
1  Knagg,  Lancet,  1907,  p.  1477. 


428  NERVOUS    DISEASES 

drowsiness  produced  by  gazing  into  a  red  fire  on  a  winter  afternoon 
is  something  entirely  different.  It  is  probably  a  mild  variety  of 
hypnotic  sleep,  the  continuous  red  glow  acting  through  the  optic 
nerves  by  a  summation  of  stimuli.  It  is  not  a  question  'of  the 
mere  heat  of  the  fire,  for  unless  the  blaze  be  seen,  drowsiness  is 
less  likely  to  supervene.  A  similar  summation  of  stimuli  probably 
explains  the  well-known  church  drowsiness.  The  soothing  mono- 
tony of  the  sermon,  combined  with  the  sitting  posture  of  the 
listener  (who  thus  has  the  additional  excuse  of  a  degree  of  cerebral 
ansemia),  and  lastly  the  common  habit  of  closing  the  eyes  to  avoid 
visual  distractions,  all  these  combine  to  make  church-drowsiness 
a  popular  disorder.  I  do  not  refer,  of  course,  to  wild  "  revival " 
meetings,  nor  to  militant  political  or  sensational  sermons,  where 
the  conditions  both  of  preacher  and  of  audience  are  entirely 
different. 

But  there  are  other  pathological  varieties  of  sleep  to  which  we 
must  refer.  There  is  the  drowsiness  of  impending  urcemic  or 
diabetic  coma,  both  toxic  in  origin.  There  is  also  that  remarkable 
tropical  disease,  sleeping-sickness,  endemic  in  certain  parts  of 
Africa,  and  associated  with  the  presence  of  trypanosomes  in  the 
blood,  glands,  and  cerebro-spinal  fluid.  The  drowsiness  in  this 
malady  is  doubtless  due  to  some  toxin  produced  by  the  parasites. 
In  the  later  stages  of  the  disease  a  peri- vascular  cellular  infiltra- 
tion is  found  around  the  cerebral  vessels,  a  variety  of  chronic 
meningo- encephalitis.  Narcolepsy  is  another  condition  where  the 
patient  has  sudden  paroxysms  of  sleep,  in  the  midst  of  whatever 
occupation  he  may  be  pursuing  at  the  moment.  These  cases  are 
hysterical.  I  remember  one  such  patient  who  used  to  fall  asleep 
when  playing  the  piano  or  during  a  game  of  cards  (especially  if  he 
held  a  losing  hand).  He  had  numerous  other  hysterical  stigmata, 
and  the  diagnosis  presented  no  serious  difficulty.  The  hypnotic 
trance  is  another  condition,  analogous  in  some  respects  to  ordinary 
sleep,  but  time  does  not  allow  us  to  discuss  it  here.  Sufiice  it  to 
say  that  the  phenomena  of  hypnosis  can  be  induced  by  repeated 
monotonous  stimuli,  visual,  auditory  or  otherwise,  aided  by  sugges- 
tion.    The  patient  is  thereby  made  to  fall  into  a  sleepy  condition. 


DISORDERS    OF    SLEEP  429 

varying  in  intensity  from  mere  drowsiness  to  dreams  (the 
incidents  of  which  are  controlled  by  suggestion),  to  somnam- 
bulisni,  or  to  deep  dreamless  slumber  lasting  perhaps  for  many 
hours.  There  are  also  the  well-known  phenomena  of  spon- 
tanams  somnavihidisin,  due  to  the  remaining  awake,  as  it  were, 
of  the  cortical  motor  centres  when  the  higher  sensory  and 
psychical  centres  have  lost  their  power  of  inhibition.  Such  a 
patient  gets  up  and  acts  his  dream.  Nightmares  are  horrifying 
dreams  which  produce  so  much  distress  that  they  sometimes 
waken  the  patient  up  in  a  state  of  dyspnoea.  They  are  generally 
toxic  in  origin.  Their  commonest  cause  is  gastro -intestinal  fermen- 
tation, certain  articles  of  diet  (proverbially  a  lobster  supper),  being 
specially  liable  to  produce  bad  dreams.  In  children  nightmares 
often  recur  again  and  again  with  the  peculiarity  that  the  terrifying 
hallucination  is  the  same  on  each  occasion.  Here  again  gastro- 
intestinal fermentation  is  often  a  factor.  Still  more  frequently  do 
we  find  that  the  child  has  adenoids,  which  interfere  with  respiration 
and  produce  a  degree  of  COg  poisoning.  Removal  of  adenoids  and 
attention  to  the  bowels  cure  most  cases  of  night-terrors  in  children. 
Patients  with  tropical  abscess  of  the  liver,  curiously  enough,  are 
particularly  liable  to  horrible  dreams,  so  much  so  that  they  may  be 
afraid  to  fall  asleep.  Here  again  the  condition  is  doubtless  toxic. 
Nightmare  is  also  a  frequent  symptom  in  patients  with  aortic 
regurgitation.  In  them  the  condition  is  not  toxic  but  vascular  in 
origin,  due  to  irregularity  in  the  blood-supply  and  to  pulsation  in 
the  cortical  capillaries. 

Lastly  let  us  consider  the  subject  of  sleeplessness  or  insomnia. 
Cases  of  insomnia  may  be  divided  into  two  great  classes,  the 
extrinsic  and  the  intrinsic. 

Extrinsic  insomnia  includes  those  cases  where  the  sleeplessness 
is  secondary  to  some  outside  cause,  not  directly  arising  in  the 
cerebrum  or  its  blood-vessels.  For  example,  physical  pain  of  any 
sort,  cough,  vomiting,  frequent  micturition,  diarrhoea,  pruritus, 
and  so  on,  may  keep  a  patient  awake.  In  all  such  cases  we  must 
treat  the  primary  symptom  ;  when  it  is  relieved,  sleep  will  follow 
naturally.     This  group  also  includes  emotional  insomnia,  which 


430  NEKVOUS    DISEASES 

is  more  often  the 'result  of  grief  than  of  joy,  and  more  commonly- 
associated  with  fear  or  apprehension  for  the-  future  than  with 
remorse  or  sorrow  for  the  past.  When  pleasui-able  emotion  does 
cause  insomnia,  it  is  generally  due  to  anticipation  of  some  happiness 
in  the  immediate  future.  A  man  does  not  usually  lie  awake  because 
some  one  is  going  to  leave  him  a  fortune  twenty  years  hence,  but 
he  may  spend  a  sleepless  night  on  the  eve  of  his  wedding.  The 
treatment  of  emotional  insomnia,  apart  from  assuaging  the  patient's 
sorrow  (a  matter  which  is  often  beyond  the  physician's  sphere), 
is  best  accomplished  by  giving  some  cerebral  sedative,  such  as 
a  mixture  of  chloral  and  potassium  bromide.  The  insomnia  of 
extreme  joy  seldom  calls  for  treatment,  but  if  the  patient  becomes 
too  excited,  here  again  a  cerebral  sedative  may  be  given. 

We  are  much  oftener  consulted  with  regard  to  the  other  kind 
of  insomnia,  which  we  may  call  intrinsic  insomnia.  This  is 
commonly  due  to  vascular,  toxic,  or  nervous  faults,  or  to  com- 
binations of  all  three. 

As  to  vascular  causes,  the  brain  may  be  hypersemic,  rendering 
sleep  impossible.  Hypereemic  insomnia  may  be  either  of  the  high- 
tension  or  of  the  low-tension  type.  In  high-tension  insonmia  the 
patient  may  be  the  subject  of  general  arterio -sclerosis  or  of  renal 
disease,  and  the  hyper-tension  is  readily  demonstrated  by  the 
Riva-Rocci  sphygmo-manometer.  In  such  cases  the  patient 
complains  of  a  difficulty  in  falling  ofi  to  sleep.  The  best  remedy, 
as  Broadbent^  urged,  is  to  give  a  mercurial  aperient  such  as 
blue  pill  or  calomel,  say  two  or  three  times  a  week.  This  often 
brings  down  the  tension  in  a  remarkable  way  and  induces  sleep. 
Of  course  we  also  lay  down  careful  regulations  as  to  diet,  &c., 
in  these  cases.  Hypereemic  insomnia  from  low  tension  occurs  in 
ansemic  and  neurasthenic  patients,  as  already  explained,  and  is 
characterised  by  the  fact  that  when  the  patient  sits  erect  in  a 
chair  he  becomes  drowsy,  whereas  when  he  lies  down  in  bed 
the  brain  becomes  over-filled  with  blood  and  the  patient  cannot 
get  to  sleep.  In  such  cases  the  best  remedy  is  a  combination  of 
a   cardio -vascular  tonic   like   digitahs   with  a   moderate   dose   of 

1  Practitioner,  July  1906. 


DISORDERS    OF    SLEEP  431 

bromide  of  potassium.  Hyperaemic  insomnia,  whether  of  high- 
tension  or  of  low-tension  type,  is  often  associated  with  cold  feet. 
If  the  feet  can  be  made  warm,  the  cerebral  hypersemia  tends  to 
become  alleviated.  A  cup  of  hot  milk  or  hot  soup,  by  producing 
abdominal  hypergemia,  often  relieves  hypersemic  insomnia. 

Insomnia  is  one  of  the  most  distressing  symptoms  of  chronic 
heart-failure.  Just  when  dropping  off  to  sleep  the  patient  suddenly 
starts  awake  with  a  feeling  of  suffocation,  gasping  for  breath. 
This  is  probably  due  to  deficient  circulation  in  the  medulla 
oblongata.  We  treat  the  condition  by  cardiac  tonics,  together 
with  one  of  the  non-depressant  pure  hypnotics,  or  even  by  morphia, 
cautiously  administered  and  combined  with  atropine. 

Next  we  have  toxic  insonmia,  which  is  one  of  the  commonest 
varieties  met  with  in  practice.  Many  cases  are  associated  with 
gastric  or  intestinal  fermentation,  and  especially  with  dilatation 
of  the  stomach.  The  symptoms  are  characteristic.  The  patient 
falls  asleep,  but,  after  an  hour  or  two,  varying  according  to  the 
degree  of  gastric  dilatation,  he  wakes  up,  perhaps  after  a  horrible 
dream,  with  palpitation,  profuse  sweating  or  gastric  uneasiness. 
He  may  have  a  sinking  feeling  with  craving  for  food,  and  if  he 
eats  a  biscuit  or  some  other  simple  food,  the  stomach  contents 
are  temporarily  diluted  and  he  feels  relieved  for  the  time.  This 
may  mislead  him  into  thinking  that  his  sleeplessness  is  due  to 
exhaustion  from  want  of  food,  which  is  far  from  the  fact.  During 
his  waldng  hours  he  is  often  very  depressed,  hypochondriac,  and 
almost  melancholic.  When  we  have  a  clinical  history  of  this 
sort,  we  should  carefully  examine  the  abdomen.  If  we  find  the 
physical  signs  of  dilated  stomach,  we  treat  the  patient  accordingly, 
putting  him  on  a  dry  dietary,  free  from  starchy  foods  or  green 
vegetables,  and  attending  carefully  to  the  bowels.  We  meanwhile 
administer  gastro -intestinal  antiseptics  such  as  carbolic  acid, 
creasote,  /3  naphthol,  or  su^pho-carbolate  of  soda.  To  give  hypnotics 
in  such  cases,  without  correcting  the  gastric  condition,  is  worse 
than  useless. 

Amongst  the  toxic  forms  of  insomnia  we  must  not  omit  to 
refer  to  the  sleeplessness  produced  by  chronic  excess  in  alcohol, 


432  NERVOUS    DISEASES 

culminating  sometimes  in  delirium  tremens,  also  the  insomnia  of 
acute  fevers.  Both  in  fever  and  in  delirium  tremens,  sleep  can 
often  be  induced  by  a  cold  pack  or  cold  sponging.  Insomnia  may 
result  sometimes  from  excessive  tobacco  smoking,  which  produces 
its  effect  partly  by  its  action  on  the  nerve -cells,  partly  by  its 
influence  on  the  circulation.  Strong  tea  or  coffee  may  also  act 
in  a  similar  fashion,  keeping  a  patient  awake.  Insomnia  may 
occur  in  secondary  or  tertiary  syphilis,  even  apart  from  the 
familiar  nocturnal  headache :  this  variety  yields  promptly  to 
mercury. 

Lastly,  there  is  'primary  or  "  nervous  "  insomnia,  due  to  over- 
fatigue, especially  from  mental  over-work.  We  see  many  instances 
amongst  busy  professional  or  business  men.  But  in  most  cases 
there  are  several  factors  involved,  not  only  the  toxins  of  exhaustion 
but  those  of  hasty  and  ill-digested  meals,  together  with  a  suc- 
cession of  powerful  mental  stimuli,  and  the  persistent  cerebral 
hypersemia  of  the  brain-worker. 

In  every  case  of  primary  insomnia,  besides  correcting  any  gastric, 
intestinal,  or  vascular  fault  that  may  be  present,  we  should  make 
it  a  golden  rule  to  send  the  patient  away  for  a  complete  holiday. 
These  are  also  the  cases  for  the  employment  of  the  pure  hypnotics, - 
which  have  a  direct  sedative  action  on  the  psycho-sensory  cortex. 
The  name  of  these  drugs  is  legion,  and  I  do  not  propose  to  discuss 
them  exhaustively.  Amongst  the  most  rehable  is  paraldehyde. 
Its  somewhat  nauseous  taste  is  no  drawback,  since  it  prevents 
the  patient  from  acquiring  a  habit  for  the  drug.  Of  the  other 
hypnotics  I  need  only  mention  a  few,  such  as  chloral  hydrate, 
sulphonal,  and  veronal.  We  should  never  allow  a  patient  carte 
blanche  to  take  a  hypnotic  drug  on  his  own  initiative.  Self- 
drugging  with  hypnotics  is  highly  dangerous.  No  hypnotic  should 
ever  be  taken  without  the  express  authority  of  the  physician. 
Nor  should  any  one,  even  though  he  be  a  medical  man,  prescribe 
hypnotics  for  himself ;   he  should  call  in  a  professional  colleague. 

Drugs  like  hyoscine  and  morphia  are  our  last  resort  in  obstinate 
insomnia.  In  severe  cases  of  excited  mania  or  melancholia  gr.  x^ 
of  hyoscine,  hypodermically,  or  gr.  J  of  morphine  with  gr.  yw  of 


DISOKDERS    OF    SLEEP  433 

atropine,  soothe  the  patient  in  a  remarkable  way.  Persistent 
insomnia  in  cases  of  insanity  is  of  serious  omen.  Most  ahenist 
physicians  insist  on  having  charts  kept  of  the  amomit  of  sleep 
obtained  by  each  insane  patient,  since  severe  insomnia  recurring 
regularly  for  a  month  in  cases  of  insanity  renders  the  prognosis 
as  to  recovery  very  unfavourable. 


2  E 


CHAPTER  XXY 

INTRA-CRANIAL   TUMOURS 

For  clinical  purposes  we  include  under  tMs  heading  not  only  the 
neoplasms  proper  (glioma,  sarcoma,  endothelioma,  fibroma,  carci- 
noma, &c.),  but  also  gummatous  and  tuberculous  growths,  para- 
sitic cysts,  and  even  aneurisms  and  abscesses.  All  of  these  may  be 
regarded  as  slowly-growing  foreign  bodies  which,  sooner  or  later, 
according  to  their  situation  within  the  cranial  cavity,  produce 
clinical  phenomena  rendering  their  diagnosis  possible,  Most 
tumours  produce  their  effects  by  displacement,  distortion,  and 
compression  of  the  nerve-elements.  Only  in  a  few  instances 
{e.g.  in  carcinoma,  melanotic  sarcoma)  are  the  nerve  elements 
directly  destroyed  by  the  tumour  cells.  Two  classes  of  signs  and 
symptoms  result ;  firstly,  general  symptoms  of  increased  intra- 
cranial pressure,  independent  of  the  position  of  the  tumour,  and 
secondly,  focal  symptoms,  which  vary  according  to  the  particular 
part  of  the  brain  implicated  by  the  growth.  General  symptoms 
enable  us  to  say  that  there  is  a  tumour  somewhere  within  the 
skull ;  in  order  to  locate  the  growth  precisely,  we  must  search 
for  localising  symptoms  which  are  usually,  though  not  necessarily, 
later  in  onset.  If  localising  symptoms  are  absent,  focal  diagnosis 
may  be  impossible. 

General  Symptoms.  —  The  cardinal  phenomena  of  intra- 
cranial tumour  are  three  in  number,  viz.  headache,  optic  neuritis, 
and  vomiting.  To  these  may  be  added  others,  such  as  mental 
changes,  generalised  convulsions,  giddiness,  slowing  of  the  pulse,  &c. 
The  triad  syndrome  of  headache,  optic  neuritis,  and  vomiting  should 
always  suggest  the  possible  presence  of  an  intra-cranial  growth. 
But  before  diagnosing  cerebral  tumour  from  these  three  signs 
alone,  we  must  be  careful  to  exclude  three  other  conditions,  any 
of  which  may  produce  the  triad  syndrome.     These  conditions  are 

434 


INTRA-CRANIAL    TUMOURS  435 

kidney  disease,  severe  anaemia,  and  lead-poisoning,  all  of  them 
easy  of  recognition  if  we  bear  the  point  in  mind. 

Headache  is  the  most  constant  symptom  of  intra -cranial  tumour  ; 
it  generally  appears  at  some  period  or  other,  sooner  or  later.  Its 
severity  is  sometimes  intense.  Usually  it  is  a  constant  dull  pain 
with  paroxysms  of  agonising  intensity.  The  pain  may  be  diffuse 
or  localised.  If  localised,  its  position  does  not  necessarily  corre- 
spond with  the  situation  of  the  tumour,  except  in  tumours  at  or 
near  the  surface  of  the  brain,  where  the  pain  may  sometimes  be 
directly  over  the  growth  and  accompanied  by  local  tenderness 
on  percussion  or  pressure,  or  even  by  a  local  alteration  of  percussion- 
note.  But  too  much  stress  shouM  not  be  laid  on  the  existence 
of  locaHsed  pain,  unless  accompanied  by  other  focal  signs.  Thus, 
for  example,  cerebellar  tumours  often  produce  frontal  headache, 
and  in  one  case  of  my  own  ^  a  right-sided  cerebellar  growth  was 
accompanied  by  pain  limited  to  the  left  frontal  region.  The 
headache  of  intra-cranial  tumour  is  intensified  by  excitement,  by 
exertion,  or  by  any  temporary  cerebral  hypersemia. 

Opic  neuritis  or  "  choked  disc,"  detected  with  the  ophthalmo- 
scope, should  be  looked  for  in  every  case  of  suspected  intra-cranial 
tumour.  But  it  should  be  borne  in  mind  that  while  the  presence 
of  optic  neuritis  is  one  of  the  strongest  evidences  of  intra-cranial 
mischief,  no  weight  should  be  laid  on  its  absence  if  other  signs 
point  to  intra-cranial  growth.  Optic  neuritis  from  brain  tumour 
is  relatively  more  frequent  in  hypermetropic  than  in  myopic  eyes." 
Another  point  of  importance  is  that  intense  optic  neuritis  may 
coexist  with  perfect  vision.  But  in  time,-  optic  neuritis  generally 
progresses  to  optic  atrophy,  with  its  accompanying  blindness. 
Many  patients  with  intra-cranial  tumour  have  early  transient 
blindness,  sometimes  momentary,  sometimes  lasting  for  a  few 
hours  or  days  at  a  time,  in  one  or  both  eyes.  Trephining  the 
skull  and  opening  of  the  dura  mater  relieve  optic  neuritis  even 
though  the  growth  be  not  removed  ;  they  also  give  considerable 
relief  to  the  headache.     The  optic  neuritis  of  brain  tumours,  though 

^  Edin.  Hosp.  Reports,  1895.     An  almost  identical  case  has  been  recorded 
by  Sachs  {Medical  Record,  December  22,  1906). 
2  Gunn,  Brit.  Med.  Journ.,  1907,  p.  1126. 


436  NEEVOUS    DISEASES 

generally  affecting  both,  eyes,  may  be  unequal  on  the  two  sides, 
or  it  may  even  be  monocular.  On  the  whole,  the  greater  intensity 
tends  to  be  on  the  same  side  as  the  tumour,  especially  in  frontal 
and  cerebellar  tumours,  though  this  rule  is  not  invariable.  In 
cerebellar  tumours  optic  neuritis  is  specially  early  in  onset. 

Vomiting  is  a  less  constant  phenomenon  than  headache  and 
optic  neuritis,  except  in  tumours  of  the  posterior  fossa,  in  which, 
from  the  very  outset,  it  is  rarely  absent.  "  Cerebral "  vomiting 
differs  from  the  ordinary  vomiting  of  abdominal  disorders.  It 
usually  occurs  independently  of  food,  and  is  miassociated  with 
other  gastro -intestinal  symptoms.  Moreover,  it  is  often  unpreceded 
by  nausea  and  thus  has  a  curious  "  projectile "  character.  A 
change  of  posture  of  the  head  is  sometimes  enough  to  induce  an 
attack  of  cerebral  vomiting. 

Amongst  the  other  '  general '  symptoms  we  must  mention 
progressive  mental  dulness.  This  is  apparently  to  a  large  extent 
the  result  of  increased  intra-cranial  pressure  and  of  persistent 
headache.  The  patient  becomes  apathetic,  dull,  and  slow  in 
answering  questions ;  he  loses  interest  in  his  ordinary  affairs. 
Sometimes  he  becomes  overwhelmingly  drowsy  and  finally  comatose. 
In  the  later  stages  the  sphincters  are  uncontrolled.  Mental  changes 
are  particularly  early  of  onset  in  tumours  of  the  pre-frontal  region, 
altogether  independently  of  the  intensity  of  the  headache. 

Generalised  epileptiform  convulsions  (as  distinguished  from 
Jacksonian  attacks)  may  be  produced  by  tumours  in  almost  any 
part  of  the  brain,  not  necessarily  in  the  immediate  neighbourhood 
of  the  motor  areas.  Such  convulsions  probably  result  mainly 
from  increased  intra-cranial  pressure  and,  as  a  rule,  occur  com- 
paratively late  in  the  disease.  But  they  may  also,  though  less 
commonly,  appear  as  the  initial  symptom  of  an  intra-cranial 
growth.  In  such  cases  epilepsy  is  sometimes  diagnosed,  and 
until  further  phenomena  (such  as  optic  neuritis  or  focal  signs) 
develop,  the  error  is  unavoidable.  More  usually  general  con- 
vulsions are  a  late  phenomenon,  and  there  are  antecedent  physical 
signs  to  guide  us. 

Attacks  of  giddiness  are  often  complained  of  in  brain  tumour. 


INTRA-CRANIAL    TUMOUES  437 

Sometimes  these  are  merely  indescribable  feelings  of  confusion ; 
in  other  cases  there  is  a  true  vertigo  or  feehng  of  uncertainty  in 
equilibration.  Vertigo  is  specially  early  and  severe  in  tumours  of 
the  cerebellum,  cerebellar  peduncles,  and  corpora  quadrigemina, 
and  in  them  it  is  often  associated  with  the  motor  phenomenon  of 
a  reeling  or  staggering  gait. 

Slowing  of  the  fidse,  permanent  or  transient,  is  a  valuable 
corroborative  sign  of  intra -cranial  abscess.  It  may  also  occur  as 
one  of  the  general  symptoms  of  tumour,  especially  in  the  neigh- 
bourhood of  the  medulla  oblongata.  In  other  cases,  again,  we 
may  meet  with  tachycardia.  Therefore  the  pulse-rate  of  itself 
is  not  of  high  diagnostic  significance,  compared  with  the  other 
signs  already  mentioned.  Slowness  of  breathing  and  a  Cheyne- 
Stokes  type  of  respiration  may  occur,  but  mostly  in  the  latest 
stages  of  the  disease.  Paroxysms  of  yawning  or  of  hiccough  may 
also  be  produced  by  intra -cranial  growths,  especially  those  of  the 
posterior  fossa . 

Localising'  symptoms  are  sometimes  absent,  and  a  tumour 
may  only  be  revealed  by  post-mortem  examination.  This 
experience  is  coromoner  with  temporal  tumours  than  with  those 
occurring  elsewhere.  In  most  cases,  however,  focal  symptoms 
develop,  which  enable  us  to  determine  the  position  of  the  orowth 
with  greater  or  less  precision.  In  a  few  cases  radiography  may 
reveal  an  abnormal  shadow  in  the  position  of  the  tumour.  In 
superficial  tumours  local  percussion  of  the  skuU  may  occasionally 
yield  an  altered  note.  But  in.  some  cases  we  can  only  form  an 
approximate  idea  as  to  the  site  of  the  disease.  For  example,  if  a 
patient  with  headache,  vomiting,  and  optic  neuritis  develops  a 
gradually  increasing  left  hemiplegia,  aU  that  we  are  justified  in 
diagnosing  is  a  growth  somewhere  in  the  right  cerebral  hemi- 
sphere, probably  in  the  neighbourhood  of  the  motor  tract.  Unless 
additional  signs  appear,  it  may  be  impossible  to  say  more,  since 
such  hemiplegia  may  be  produced  not  only  by  tumours  directly 
implicating  the  pyramidal  tract,  but  also  by  frontal,  temporal,  or 
even  occipital  tumours  compressing  the  motor  path.  Again,  the 
occurrence  of  cranial  nerve  palsies  is  always  suggestive  of  a  lesion 


438  NERVOUS    DISEASES 

at  the  base  of  the  brain ;  but  this  rule  is  not  invariable.  For 
example,  isolated  ocular  palsy  of  one  external  rectus  has  little  or 
no  localising  value,  since  the  sixth  nerve  maybe  paralysed  (whether 
from  traction  or  from  increased  intra-cranial  pressure)  by  a  growth 
anywhere  within  the  skull.  Further,  we  may  have  "  false  localising 
signs "  ^  from  compression  or  distortion  by  growths  in  distant 
parts  of  the  brain.  Thus,  for  example,  a  tumour  of  the  frontal 
lobe  may  at  a  later  stage  produce  signs  of  contra -lateral  cerebellar 


Fig.  223. — Tumour  of  right  pre-central  gyrus  in  its  upper  half.  The  patient 
had  Jacksonian  fits  of  the  left  upper  and  lower  limbs  without  sensory  impair- 
ment of  the  left  limbs.     K  =  Sulcus  Rolandi ;  S  =  Fossa  Sylvii. 

disease,  or  a  cerebellar  growth  may  afterwards  be  associated  with 
Jacksonian  fits  of  one  limb,  suggestive  of  a  lesion  of  the  motor 
area,  but  really  due  to  distension  of  the  lateral  ventricle  of  the 
corresponding  side,  and  so  on.  Or  again,  localising  symptoms 
may  be  masked  or  concealed,  as  in  some  occipital  tumours  in  which, 
if  the  optic  neuritis  goes  on  to  atrophy  and  blindness,  the  hemi- 
anopia  becomes  lost  which  might  have  led  to  a  correct  diagnosis. 
Localising  signs,  to  be  of  value,  should  generally  be  early.  Ab- 
sence of  local  signs  suggests  that  the  tumour  is  above  the  tentorium, 
since  sub-tentorial  growths  almost  always  produce  localising  signs 
early  in  their  course. 

1   Collier,  Brain,  1901,  p.  490, 


INTRA-CRANIAL    TUMOURS  439 

Bearing  the  above  points  in  mind,  let  us  now  consider  the  chief 
localising  symptoms  of  tumours  in  the  various  regions  of  the  brain. 
Tumours  of  the  Motor  Cortex. — The  motor  area,  as  we  have 
already  seen,  comprises  the  pre-central  convolution  and  the  ad- 
jacent end  of  the  second  frontal  gyrus,  together  with  part  of  the 
cortex  on  the  mesial  surface  of  the  hemisphere.  Tumours  of  the 
motor  region  are  the  easiest  of  all  to  recognise  clinically.  In  them, 
in  addition  to  the  general  signs  of  intra -cranial  tumour,  we  usually 
observe  two  classes  of  phenomena,  irritative  and  paralytic. 

The  irritative  group  consists  of  Jacksonian  fits,  commencing  in 
the  contra -lateral  face,  tongue,  arm,  or  leg,  as  the  case  may  be, 
accordmg  to  the  part  of  the  motor  cortex  which  happens  to  be 
chiefly  implicated.  In  a  Jacksonian  fit  the  convulsion,  generally 
consisting  of  tonic  spasm  followed  by  clonic  jerks,  may  be  strictly 
localised  to  a  small  group  of  muscles,  or  it  may  spread  from  them 
to  other  muscle-groups,  but  always  in  a  regular  order  (as  shown 
in  Fig.  3,  p.  5).  Less  commonly  the  whole  of  the  muscles  of 
the  contra -lateral  face,  arm,  and  leg  are  thrown  into  convulsion 
simultaneously.  During  Jacksonian  convulsions,  unhke  ordinary 
epilepsy,  the  patient  usually  retains  consciousness  all  the  time, 
and  can  study  his  own  fit.  But  if  the  convulsion  spreads  across 
the  middle  line  and  becomes  bilateral,  consciousness  becomes  lost 
at  or  before  the  moment  of  crossing. 

The  'paralytic  phenomena  in  tumours  of  the  motor  region  consist 
in  weakness  of  the  convulsed  muscles  during  the  inter-paroxysmal 
periods  (see  Figs.  31  and  32,  p.  72).  Such  weakness  is  most 
marked  immediately  after  a  con\->ulsion.  There  is  also  temporary 
atopognosis  in  the  afiected  limb  and  loss  of  the  sense  of  position. 

According  as  the  growth  is  primarily  cortical  or  sub-cortical, 
convulsions  precede  muscular  weakness  or  vice  versa.  A  cortical 
tumour,  for  example  one  growing  from  the  meninges,  is  irritative 
from  the  first ;  a  sub-cortical  growth  is  usually  indicated  by  an 
initial  monoplegia,  followed  later  by  Jacksonian  con^iilsions. 
Moreover,  the  precise  starting-point  of  the  convulsions  in  a  sub- 
cortical growth  is  less  constantly  localised  to  the  same  muscle - 
group ;    thus,   for   example,   a   sub-cortical  tumour   inmiediately 


440  NERVOUS    DISEASES 

under  the  arm-area  may  produce  Jacksonian  fits,  commencing 
sometimes  in  the  thumb,  at  other  times  in  the  elbow.  The  extent 
of  a  Jacksonian  fit  also  varies  with  the  extent  of  the  tumour.  A 
small  superficial  tumour  will  produce  a  highly  localised  fit  followed 
by  monoplegia  of  the  affected  part,  whereas  a  tumour  of  the  same 
size,  situated  deeper  beneath  the  cortex,  will  produce  an  initial 
monoplegia,  convulsions  being  weeks  or  months  later  in  onset. 
The  deeper  the  growth,  the  less  tendency  is  there  to  localised  con- 
vulsions. Tumours  of  the  pre-central  or  motor  area,  if  extending 
backwards  across  the  Rolandic  fissure  to  the  post-central  convolu- 
tion, are  usually  associated  with  a  distinct  sensory  aura  in  the 
affected  limb  at  the  beginning  of  the  motor  convulsion,  together 
with  a  degree  of  anaesthesia,  monoplegic  or  hemiplegic  in  distribu- 
tion. The  differences  between  cortical  and  sub-cortical  types  of 
anaesthesia  have  already  been  discussed  (p.  200). 

Tumours  of  the  Frontal  Region. — ^For  clinical  purposes  this 
region  of  the  brain-cortex,  anterior  to  the  motor  area  proper,  may 
be  subdivided  into  two  parts  :  (1)  A  pre-f rental  or  higher  psychical 
area,  devoid  of  motor  centres.  This  area,  when  electrically 
stimulated,  produces  no  convulsion.  (2)  A  post-frontal  area,  con- 
tinuous posteriorly  with  the  pre-central  convolution  and  including - 
the  cortical  centre  for  conjugate  deviation  of  the  head  and  eyes 
towards  the  opposite  side.  On  the  left  side  it  contains,  in  addi- 
tion, the  cortical  motor  centres  for  spoken  words. 

Pre-frontal  tumours,  besides  having  the  general  signs  of 
cerebral  tumour,  tend  to  exhibit  mental  symptoms  specially  early, 
consistiug  in  dulness,  failure  of  memory,  tendency  to  childish 
jocularity,  deficiency  of  attention,  and  neglect  of  the  sphincters. 
These  mental  symptoms  are  equally  likely  in  tumours  of  the 
right  side  and  of  the  left.-^  Some  pre-frontal  tumours,  however, 
have  no  mental  symptoms  at  all.  Post-frontal  tumours  have,  in 
addition,  local  Jacksonian  fits,  especially  attacks  beginning  with, 
or  consisting  entirely  in,  deviation  of  the  head  and  eyes  to  the 
contra-lateral  side  ;  also,  in  left-sided  tumours,  fits  commencing 
with  sudden  attacks   of  motor  aphasia   (though  the  absence   of 

^  Beevor,  Lettsomian  Lectui'es,  1907. 


INTRA-CKANIAL    TUMOURS  441 

aphasia  does  not  necessarily  exclude  a  diagnosis  of  left-sided  post- 
frontal  growth).  General  epileptiform  convulsions,  and  even 
attacks  of  petit  mal,  are  not  uncommon  in  frontal  tumours,  in- 
cluding pre-frontal  cases.  Tumours  beginning  on  the  under  or 
orbital  surface  of  the  frontal  lobe  may  also  be  associated  with 
early  and  persistent  anosmia  on  the  ipso -lateral  side,  from  im- 
plication of  the  olfactory  bulb  and  tract.  Difficulty  in  moving 
the  head  and  eyes  to  the  contra -lateral  side  would  point  to  a  sub- 
cortical mid-frontal  growth.  Frontal  tumours,  whether  pre-  or 
post-frontal,  are  sometimes  associated  with  a  fine  vibratory 
tremor  of  the  ipso -lateral  arm,  and  less  markedly  of  the  leg,  on 
holding  the  Hmbs  outstretched^  (though  this  is  far  from  con- 
stant), and  with  loss,  or  speedy  exhaustion,  of  the  contra -lateral 
superficial  reflexes,  especially  the  abdominal  and  epigastric.  If 
the  growth  be  sufficiently  extensive  to  press  baclrw^ards  on  the 
pyramidal  tract,  there  may  be  an  increase  in  the  contra -lateral 
deep  reflexes,  with  an  extensor  plantar  reflex  in  the  contra- 
lateral foot,  and  even  a  degree  of  motor  hemi-paresis.  Optic 
neuritis,  generally  late  in  onset,  tends  to  be  more  intense  on 
the  side  of  the  tumour,  whilst  local  tenderness  and  alteration  of 
percussion-note  are  relatively  common.  Some  cases  of  frontal 
tumour  are  associated  with  a  reeling  gait,  like  that  of  cerebellar 
disease  ;  whether  this  is  due  to  backward  displacement  of  the 
brain,  producing  compression  of  the  cerebellum,  or  to  the  trans- 
mission of  abnormal  impulses  along  the  crossed  fronto-c3rebellar 
path,  is  at  present  difiicult  of  decision. 

Tumours  of  the  Temporal  Lobe  are  the  most  difficult  of  all 
to  localise,  especially  right-sided  tumours.  This  is  because  their 
symptoms  are  produced  chiefly  by  pressure  on  adjacent  parts, 
and  only  to  a  lesser  extent  by  true  focal  lesions.  There  are,  how- 
ever, two  focal  symptoms  which  are  of  diagnostic  value.  Firstly, 
tumours  at  the  tip  of  the  lobe,  in  the  region  of  the  uncinate  gyrus, 
are  often  associated  with  sudden  attacks  commencing  with  an 
olfactory  or  gustatory  sensation,  the  smell  being  usually  an  un- 
pleasant one.  This  aura  is  followed  by  a  curious  "  dreamy  state," 
^  Grainger  Stewart,  Lancet,  November  3,  1906. 


442  NERVOUS   DISEASES 

lasting  several  seconds,  during  which,  everjrthing  seemsi  to  the 
patient  to  be  unreal  or  "  far  away."  These  "  uncinate  fits  "  are 
occasionally  accompanied  by  smacking  movements  of  the  lips. 
Secondly,  tumours  of  Heschl's  convolution  (on  the  Sylvian  surface 
of  the  lobe)  and  of  the  adjacent  first  temporal  gyrus,  if  on  the  left 
side,  may  produce  word-deafness.  But  many  temporal  tumours 
are  totally  devoid  of  focal  symptoms  and  only  produce  symptoms 
of  pressure  on  neighbouring  parts.  Thus  pressure  on  the  internal 
capsule  may  cause  a  slight  hemiplegia,  with  its  accompanying 
disordered  reflexes.  Or  tumours  of  the  antero -internal  aspect  of 
the  lobe  may  implicate  the  optic  tract,  or  may  extend  to  the  crus 
cerebri,  or  to  the  corpora  quadrigemina,  producing  corresponding 
symptoms. 

Tumours  of  the  Post-central  Convolution. — Here  the  focal 
symptoms  of  a  cortical  growth  consist  of  attacks  commencing 
with  a  sensory  aura  either  of  tingling  or  of  pain  in  the  opposite  face, 
arm,  or  leg,  according  to  the  position  of  the  irritative  lesion.  If 
the  growth  extends  across  the  fissure  of  Rolando  to  the  pre -central 
or  motor  convolution  (or  even  in  many  cases  where  the  pre-central 
convolution  is  not  actually  invaded  but  only  compressed),  there  is, 
in  addition,  a  motor  spasm  of  the  corresponding  part.  Both  in 
cortical  and  in  sub-cortical  tumours  of  the  post-central  convolu- 
tion there  is  usually  anaesthesia,  monoplegic  or  hemiplegic,  and 
of  cortical  or  capsular  type  as  the  case  may  be  (see  p.  200). 
Astereognosis  in  the  contra -lateral  hand  has  also  been  recorded, 
as  in  a  case  of  my  own.^ 

Tumours  of  the  Supra-marginal  and  Angular  Convolutions. 
— General  symptoms  are  usually  late  in  onset.  The  chief  focal 
symptoms  are  due  to  affection  of  the  visual  paths.  In  left-sided 
cases,  implicating  the  angular  gyrus,  word-blindness  may  occur  ; 
in  irritative  lesions  this  is  transitory,  in  destructive  or  sub -cortical 
lesions  it  is  permanent.  A  superficial  tumour  limited  to  the  angular 
gyrus  may  produce  "  crossed  amblyopia  "  (see  p.  38).  Thus  a 
lesion  of  the  right  angular  gyrus  produces  concentric  contraction 
of  the  visual  field  of  the  left  eye  (see  Fig.  52,  p.  122).     Such  cases 

1  Rev.  of  Neurol,  and  Psychiatry,  1908,  p.  379. 


INTRA-CEANIAL    TUMOURS  443 

are  uncommon,  but  have  been  occasionally  recorded. '^  More 
usually  the  growth  dips  in  so  as  to  affect  the  underlying  optic 
radiations,  and  then  hemianopia  results  in  the  contra -lateral  half 
of  both  visual  fields.  Hemi-ansesthesia  and  hemi-analgesia  may 
be  present  in  addit'on,  when  the  posterior  end  of  the  internal 
capsule  is  affected  ;   motor  hemiplegia  is  uncommon. 

Tumours  of  the  Postero-parietal  Lobule  are  sometimes  said 
to  be  characterised  by  astereognosis  in  the  contra-lateral  hand."  In 
such  cases  the  patient  cannot  recognise  the  form  and  qualities  of 
common  objects  placed  in  his  hand  if  his  eyes  are  closed,  whereas 
with  the  healthy  ipso -lateral  hand  he  recognises  them  at  once. 
But  stereognosis  is  a  complex  intellectual  function,  a  judgment 
based  on  many  sensory  factors,  and  astereognosis  has  also  been 
observed  in  other  conditions,  as  in  disease  of  the  post-central  gyrus, 
of  the  optic  thalamus,  of  the  posterior  spinal  nerves  and  of  the 
peripheral  sensory  nerves. 

Tumours  of  the  Occipital  Region. — This  area  of  the  brain  is 
associated  with  the  half -vision  centre.  The  cortical  half -vision 
centre  is  situated  mainly  on  the  mesial  aspect  of  the  occipital  lobe, 
partly  above  and  partly  below  the  calcarine  fissure.  The  lower 
quadrant  of  the  half-field  is  represented  above  the  fissure,  i.e.  in 
the  cuneate  lobule,  the  upper  quadrant  is  below  the  fissure,  i.e. 
in  the  lingual  gyrus.  Tumours  of  this  region,  therefore,  produce 
as  their  most  constant  symptom  half-blindness  or  hemianopia, 
which  may  be  complete  or  incomplete  (quadrantic),  according  as 
the  whole  of  the  cortical  centre  is  affected  or  only  part  above  or 
below  the  calcarine  fissure.  Wernicke's  hemiopic  pupillary  pheno- 
menon (see  p.  130)  is  absent  in  hemianopia  from  occipital  lesions. 
Tumours  on  the  surface  produce  irritative  phenomena,  whilst  those 
extending  deeper,  into  the  optic  radiations,  produce  paralytic 
symptoms.  The  irritative  phenomena  consist  of  crude  subjective 
visual  hallucinations,  such  as  luminous  sparks  or  flashes  of  light,  in 
the  contra -lateral  halves  of  the  visual  fields  of  both  eyes,  or  in  that 
part  of  the  half -field  corresponding  to  the  area  of  cortex  affected. 

1  Beevor,  Lancet,  1907,  p.  719. 

2  Cf.  a  case  by  Edwards  and  Cotterill,  Rev.  of  Neurol,  and  Psychiatry, 
1911,  p.  157. 


444  NERVOUS   DISEASES 

Such  luminous  sensations  are  usually  followed  by  hemianopia  in 
the  same  area  of  the  visual  field,  a  liemianopia  at  first  transient, 
but  which  may  become  permanent.  Tumours  of  the  cuneate  and 
lingual  gyri  may  also  press  downwards  on  the  cerebellum,  in 
which  case  cerebellar  phenomena  are  superadded. 

Let  us  now  pass  to  the  consideration  of  tumours  deep  within 
the  substance  of  the  brain.  These  are  more  difficult  to  localise 
than  in  the  case  of  cortical  growths. 

To  distinguish  between  growths  in  the  Corona  Radiata  and  those 
in  the  Internal  Capsule  is  often  difficult,  especially  when  the  tumour 
is  a  large  one.  All  that  it  may  be  possible  to  state  is  that  the 
tumour  is  somewhere  in  one  cerebral  hemisphere.  But  with  less 
extensive  growths,  producing  less  complete  hemiplegia,  the  degree 
of  paralysis  of  different  limbs  is  of  diagnostic  value.  Thus  the 
closer  a  lesion  is  situated  to  the  cortex,  the  greater  is  the  tendency 
towards  a  monoplegia.  Also  if  there  be  a  hemiplegia  which  is 
complete  in  the  lower  limb  but  incomplete  in  the  upper,  and  if 
we  find  that  the  hand  is  more  affected  than  the  shoulder,  this 
would  point  to  a  capsular  lesion  rather  than  a  sub-cortical  one, 
since  in  the  cortex  the  shoulder  centre  is  the  one  nearest  to  that 
for  the  lower  limb  (see  Figs.  3  and  7). 

Tumours  of  the  Central  Ganglia — In  this  region  growths  may 
develop  without  producing  enough  focal  symptoms  to  render 
locahsation  possible.  From  the  close  proximity  of  the  optic 
thalamus  and  corpus  striatum  to  the  motor,  sensory,  and  visual 
paths  in  the  internal  capsule,  a  slowly  progressive  hemi-paresis 
or  hemiplegia  may  occur,  accompanied  by  hemianopia  and  a 
degree  of  hemi-ansesthesia.  But  if  these  phenomena  be  present, 
say  on  the  right  side,  and  nothing  more,  beyond  the  general  signs 
of  intra-cranial  tumour,  all  that  we  can  diagnose  is  a  growth  some- 
where within  the  left  cerebral  hemisphere,  and  probably  in  its 
posterior  two-thirds.  But  sometimes  we  can  be  more  precise. 
For  example,  Nothnagel  long  ago  showed  that  the  optic  thalamus 
is  a  lower  reflex  centre  for  the  emotional  movements  of  laughing 
and  crying,  and  cases  of  thalamic  lesion  have  been  demonstrated 
where  voluntary  movements   of  the  face  were  preserved  whilst 


INTRA-CKANIAL    TUMOUES  445 

emotional  movements  were  impaired  or  lost  on  the  contra -lateral 
side  of  the  face.  Further,  a  small  lesion  in  the  lower  and  posterior 
part  of  the  thalamus  may  cause  (probably  from  affection  of  the 
adjacent  rub ro -spinal  path)  spontaneous  slow  rhythmic  move- 
ments of  the  contra -lateral  limbs,  athetoid  or  choreiform,  increased 
on  voluntary  exertion.  The  plantar  reflex  in  these  cases  remains 
flexor  in  type,  provided  the  internal  capsule  be  not  involved. 
Again,  the  optic  thalamus,  as  we  have  already  seen,  is  an  important 
station  in  the  general  sensory  path,  and  therefore  sensory  symptoms 
are  sometimes  prominent,  especially  subjective  sensations  of  pain, 
heat,  and  cold,  in  the  contra -lateral  side  of  the  body,  together  with 
a  degree  of  hemi-ansesthesia.  Many  cases  of  thalamic  tumour,  how- 
ever, run  their  course  without  any  sensory  impairment  whatever. 

Tumours  of  the  Corpus  Callosum  have  no  focal  symptoms 
which  can  be  regarded  as  pathognomonic.  Tumours  in  the  anterior 
part  of  this  great  commissure  generally  produce  early  mental 
symptoms,  to  which  may  be  superadded  unilateral  or  bilateral 
hemi-paresis  or  convulsions  (cranial-nerve  palsies,  as  a  rule,  being 
absent).  But  these  symptoms  may  be  the  result  of  extension  into 
neighbouring  parts,  so  that  to  diagnose  a  callosal  growth  is  always 
hazardous.  Moreover,  it  is  rare  for  a  tumour  to  be  limited  to  the 
corpus  callosum  without  extension  into  one  or  both  hemispheres. 
Attention  has  been  drawn  to  the  occurrence  of  apraxia  (inability 
to  perform  certain  movements  when  there  is  no  actual  paralysis 
of  the  limb)  in  callosal  lesions.^      (See  p.  106 j. 

Marchiafava  "^  has  described  a  peculiar  degeneration  of  certain 
commissural  tracts  of  the  corpus  callosum  in  chronic  alcoholism. 

Tumours  of  the  Corpora  Quadrigemina  (and  of  the  Pineal 
Body  which  lies  in  close  apposition)  are  localised  with  comparative 
ease  by  the  presence  of  characteristic  ocular  phenomena.  These 
consist  in  a  paralytic  affection  of  the  third  nerve  nuclei,  more  or 
less  symmetrically  on  the  two  sides.  The  commonest  sign  is  a  com- 
bination of  bilateral  ptosis  with  weakness  of  upward  and  downward 
movements    of   the    eyes   and   feebleness   of   convergence.       The 

^  S.  A.  K.  Wilson,  Brain,  1908,  p.  164;  also  Lippmann,  Archiv.  fur 
PsycMatrie,  1908,  xliii. 

^  Eendie  della  R.  Accad.  dei  Lincei,  1910,  xiv.,  series  5,  fasc.  3. 


U6  NERVOUS    DISEASES 

pupillary  reflex  may  be  sluggish  or  absent.  Certain  tumours, 
especially  teratomata  of  the  pineal  body,  which  occur  in  children, 
are  associated  with  excessive  growth  of  the  body,  precocious  sexual 
development  and  abnormal  growth  of  the  penis  and  pubic  hairs, 
also  with  mental  precocity,  (These  signs  are  in  addition  to  the 
ocular  phenomena  above  described.)  In  this  respect  they  contrast, 
as  we  shall  presently  see,  with  certain  tumours  of  the  pituitary  body 
where  the  genital  functions  may  be  diminished.  Less  constantly, 
in  unilateral  quadrigeminal  disease,  a  degree  of  deafness  has  been 
noted  in  the  ear  of  the  opposite  side,  the  sub -cortical  auditory 
centre  being  located  in  the  posterior  corpus  quadrigeminum.  If 
the  superior  cerebellar  peduncle,  which  is  in  close  proximity,  be 
also  implicated,  we  have  a  corresponding  cerebellar  asynergia  or 
ataxia  and  reeling  gait,  while  if  the  adjacent  external  geniculate 
body  or  optic  radiations  be  involved,  there  is  hemianopia. 

Tumours  of  the  Tegmental  Region  of  the  Crus  or  Pons 
produce  characteristic  focal  symptoms  from  implication  of  the  rubro- 
spinal tract  (Monakow's  bundle)  which  starts  from  the  red  nucleus, 
runs  down  in  the  pons,  crosses  the  middle  line  and  traverses  the 
antero -lateral  column  on  the  opposite  side  of  the  spinal  cord. 
Lesions  in  the  crural  or  pontine  part  of  this  tract  produce  a  slow 
rhythmic  tremor  of  the  contra -lateral  hand  and  foot,  somewhat 
like  that  of  paralysis  agitans,  increased  by  voluntary  exertion  or 
excitement  and  ceasing  during  sleep.  If  the  lesion  be  in  the  red 
nucleus  itself,  which  is  transfixed  by  the  fibres  of  the  third  nerve, 
we  have,  in  addition,  third-nerve  palsy  of  the  ipso-lateral  side 
with  tremor  of  the  contra -lateral  arm  and  leg  —  a  condition 
known  as  "  Benedikt's  syndrome."  If  the  growth  implicates 
the  sensory  tract  of  the  fillet,  there  may  be  hemi-ansesthesia  of 
the  contra -lateral  side  of  the  body,  but  this  is  less  common  with 
tumours  than  with  sudden  vascular  lesions  such  as  haemorrhage,  &c. 

A  Tumour  of  the  Crusta  or  Ventral  Region  of  the  Crus 
Cerebri  is  easy  of  recognition,  from  the  characteristic  alternate  par- 
alysis which  is  produced,  consisting  in  third  nerve  palsy,  generally 
incomplete,  on  the  ipso-lateral  side,  with  hemiplegia  of  the  contra- 
lateral  face,  arm,  and  leg — "Weber's  syndrome"   (see  Fig.  91, 


INTRA-CEANIAL    TUMOURS  447 

p.  217).  As  the  tumour  increases  in  size,  it  tends  to  cross  the 
middle  line  and  implicate  the  opposite  third  nerve  as  well. 

Pituitary  Tumours  produce  diagnostic  symptoms  in  two 
entirely  different  ways.  Firstly,  we  may  have  signs  of  disordered 
activity  of  the  pituitary  gland  itself.  Excessive  activity  of  the 
gland  influences  the  growth  of  the  bones  throughout  the  body, 
producing  acromegaly  or  gigantism  (according  to  whether  the 
epiphyseal  cartilages  have  become  ossified  or  not).  But  skeletal 
changes  are  not  constant.  They  seem  to  occur  chiefly  in  cases  of 
adenomatous  growth,  accompanied  by  hyper-activity  of  the  gland, 
and  not  in  purely  destructive  lesions  as  in  the  sarcomata. 
Diminished  activity,  on  the  other  hand,  produces  the  so-called 
"  adiposo-genital  degeneration,"  evidenced  by  an  excessive  deposit 
of  fat  throughout  the  body,  together  with  absence  of  sexual  develop- 
ment if  the  process  dates  from  childhood,  or  regression  from  sexual 
maturity  if  the  disease  appears  in  adult  life.  Thus  in  female 
patients  we  may  observe  amenorrhoea,  whilst  an  adult  male  patient 
develops  a  remarkable  tendency  to  approximate  to  a  female  type  ; 
the  mammary  glands  enlarge,  the  testicles  diminish  in  size,  the 
abdomen  becomes  rounded  like  a  woman's,  and  the  pubic  hair 
becomes  restricted  in  area — "  pituitary  eunuchism,"  ^  accompanied 
by  loss  of  virility. 

Secondly,  and  more  constantly,  there  are  focal  symptoms  pro- 
duced by  pressure  on  adjacent  parts,  notably  on  the  optic  chiasma. 
Bi-temporal  hemianopia,  with  a  hemiopic  pupil-reaction,  results. 
This  may  afterwards  progress  to  total  blindness  of  one  eye  with 
temporal  hemianopia  of  the  other  (see  p.  124).  Curiously  enough, 
in  pituitary  tumours  primary  optic  atrophy  is  commoner  than  optic 
neuritis.  A  growth  in  the  pituitary  gland  may  also  press  back- 
wards on  the  third  nerves,  causing  ocular  palsies,  or  it  may  extend 
upwards  towards  the  floor  of  the  third  ventricle,  in  which  case  we 
sometimes  note  persistent  somnolence.  The  diagnosis  of  pituitary 
tumour  can  occasionally  be  confirmed  by  radiography,  which  may 
show  deepening  of  the  sella  turcica.     Glycosuria  is  not  uncommon. 

Tumours  of  the  Cerebellum  and  Cerebellar  Peduncles. — The 

^  Nonne,  Neurologisches  Gentralhlatt,  1907,  s.  735. 


448  NERVOUS   DISEASES 

anatomical  connections  of  the  cerebellum  are  all-important,  and 
should  be  carefully  borne  in  mind  (see  pp.  21  to  24).  Of  all  intra- 
cranial tumours,  those  of  the  cerebellum  are  the  most  frequent. 
Intra -cerebellar  growths  are  usually  tuberculous  or  gliomatous, 
whereas  extra-cerebellar  growths,  commonly  situated  in  the  ponto- 
cerebellar angle  of  the  posterior  fossa,  if  arising  from  the  ventral 
surface  of  the  cerebellum,  are  generally  gliomata,  and  if  arising 
from  the  sheaths  of  cranial  nerves  (especially  the  auditory  nerve) 
they  are  most  commonly  fibro-myxomata. 

Vertigo,  a  reeling  gait  uninfluenced  by  closure  of  the  eyes, 
nystagmus,  and  early  optic  neuritis  are  the  outstanding  symptoms 
common  to  growths  anywhere  in  the  cerebellum,  but  a  closer  study 
usually  enables  us  to  localise  the  lesion  more  exactly. 

Tumours  of  the  lateral  lobe,  whether  intra-  or  extra-cere- 
bellar, produce  symptoms  in  the  ipso-lateral  arm  and  leg  ;  these 
consist  in  paresis  and  diminished  muscular  tonus,  with  flaccid, 
flail-like  muscles,  together  with  asynergia  on  voluntary  movement, 
more  evident'  in  the  arm  than  in  the  leg.  In  the  upper  limb  we 
sometimes  observe  slowness  of  diadochokinesia,  a  term  applied  by 
Babinski  ^  to  rapid  alternate  pronation-supination  movements  of 
the  forearm.  In  lateral-lobe  tumours,  this  is  performed  slowly, 
and  awkwardly  {dys -diadochokinesia)  on  the  ipso-lateral  side. 
With  this  the  ipso-lateral  limbs  are  often  unnaturally  steady 
when  held  actively  extended  in  the  air ;  this  is  best  seen  in  the 
lower  limb  (the  patient  meanwhile  lying  on  his  back).  If 
the  patient  tries  to  stand  on  one  leg,  he  does  so  less  securely 
on  the  affected  side.  He  lurches  or  reels  as  he  walks,  sometimes 
towards  the  side  of  the  lesion,  sometimes  away  from  it.  This 
lurching  appears  to  be  due  largely  to  weakness  of  the  spinal 
muscles.  There  is  often  weakness  of  conjugate  movement  of  the 
eyes  towards  the  side  of  the  lesion,  together  with  horizontal 
nystagmus,  which  is  coarser  on  looking  towards  the  ipso-lateral 
side.  The  patient  has  a  subjective  vertigo  in  which  surrounding 
objects  appear  to  rotate  towards  the  contra -lateral  side.  The  con- 
dition of  the  deep  reflexes  is  inconstant ;  they  may  be  diminished, 
1  Revue  Neurologique,  1903,  p.  1013. 


INTRA-CRANIAL    TUMOURS 


449 


normal,  or  exaggerated  in  the  ipso-lateral  limbs.  In  some  cases 
there  is  a  characteristic  posture  of  the  head  (see  Fig.  141,  p.  286), 
the  ear  being  tilted  towards  the  contra -lateral  shoulder,  and  the 
face  slightly  turned  towards  the  ipso-lateral  side. 

According  as  the  growth  is  extra-  or  intra-cerebellar,  certain 
additional  phenomena  can  be  recognised.    Extra- cerebellar  growths 


Fig.  224. — Bilateral  auditory-nerve  tumours  (A  and  B)  in  ponto-cerebellar  angles. 
An  attempt  was  made  to  remove  the  larger  tumour  (B)  by  operation,  hence 
the  laceration  of  the  corresponding  lateral  lobe  of  the  cerebellum. 


most  frequently  arise  at  the  ponto-cerebellar  angle  from  the 
sheath  of  the  auditory  nerve  and  are  consequently  associated  with 
nerve-deafness,  more  or  less  complete,  on  the  affected  side,  usually 
accompanied  by  tinnitus  and  with  loss  of  thermic  reflex  vestibular 
nystagmus  (see  p.  134).  To  these  is  frequently  added  paresis 
of  the  facial  nerve,  a  sign  of  great  value  when  present.  Less 
commonly  we  may  have  affection  of  other  cranial  nerves,  such  as 

2  F 


450  NERVOUS    DISEASES 

the  sixth  or  fifth,  with  loss  of  corneal  reflex,  on  the  same  side. 
In  intra-cerebellar  tumours,  on  the  other  hand,  deafness  is  not 
an  essential  symptom.  The  plantar  reflexes  in  pm-e  intra- 
cerebellar  growths  are  unaltered,  whereas  in  extra-cerebellar 
cases,  from  pressure  on  the  p3rramidal  tracts,  there  may  be 
exaggeration  of  deep  reflexes  on  one  or  both  sides,  together 
with  an  extensor  type  of  plantar  reflex,  but  this  is  far  from 
constant.  In  some  intra-cerebellar  cases  the  subjective  sense  of 
rotation  felt  by  the  patient  is  the  same  in  its  direction  as  that  of 
the  apparent  rotation  of  outside  objects,  viz.,  towards  the  contra- 
lateral side.  In  extra-cerebellar  cases  this  is  sometimes  reversed, 
and  the  patient  may  have  a  subjective  sensation  of  rotation 
towards  the  ipso -lateral  side.^  Some  cases  of  tumour  of  the  lateral 
lobe  or  of  the  middle  cerebellar  peduncle  are  associated  with  spon- 
taneous "  forced  rotatory  movements  "  around  the  long  axis  of  the 
body,  analogous  to  those  produced  by  experimental  stimulation 
(see  p.  55).  Thus  in  one  case  of  my  own,  where  there  was  a  large 
sarcoma  of  the  right  lateral  lobe,  the  patient  rolled  round  per- 
sistently to  the  right  side  and  occasionally  fell  over  the  right  edge 
of  his  bed.  Unfortunately  the  direction  of  rotation  is  not  so 
constant  as  to  be  of  absolute  diagnostic  value  in  determining  the 
side  of  the  lesion ;  but  when  the  phenomenon  occurs,  it  is  a 
valuable  corroborative  sign,  indicating  an  affection  of  one  middle 
peduncle. 

Tumours  of  the  Vermis  or  middle  lobe  have  the  general 
symptoms  of  cerebellar  growth — vertigo,  reeling,  nystagmus — 
without  unilateral  preponderance  of  ataxia  on  either  side,  until 
the  growth  extends  into  one  or  other  lateral  lobe.  There  is  also 
a  tendency  to  fall  forwards  or  backwards,  according  as  the  growth 
is  situated  in  the  anterior  or  posterior  part  of  the  vermis. 

In  a  few  cases,  both  in  middle  lobe  and  in  lateral  lobe  tumours, 
we  may  observe  "  cerebellar  fits  "  of  a  tonic  type  (see  p.  77). 

It  should  be  noted  that  asynergia  is  not  necessarily  present  in 

^  This  alleged  difference  between  intra-  and  extra-cerebellar  tumours  as 
regards  subjective  sense  of  rotation  is  doubted  by  Oppenheim  and  by  other 
competent  observers.    It  is  therefore  too  uncertain  to  be  conclusive  by  itself . 


INTRA-CEANIAL    TUMOURS 


451 


all  cases  of  cerebellar  disease.  Sometimes  its  absence  is  due  to 
compensation  by  other  parts  of  the  brain,  and  some  cases  are 
instances  of  lesions  limited  to  the  white  matter  at  a  distance  from 
the  cortical  or  central  nuclei  and  their  main  connecting  paths. 
Asynergia  is  most  constantly  present  in  lesions  implicating  the 
posterior  part  of  the  vermis. 

Tumours  of  the  Pons. — In  this  region  focal  symptoms  usually 
appear    early,  but   general    symptoms,  especially   optic    neuritis, 


Fig.  225.  —  Sarcoma  occupying  centre  of  pons. 

tend  to  be  late  in  onset.  The  most  characteristic  sign  of  a  uni- 
lateral pontine  lesion  is  an  "  alternate  "  paralysis  of  the  fifth, 
sixth,  or  seventh  cranial  nerve  or  nucleus  on  the  ipso -lateral 
side,  together  with  hemiplegia  of  the  contra -lateral  arm  and  leg 
and  an  extensor  plantar  response,  or,  if  the  growth  be  situated  in 
the  dorsal  region  of  the  pons,  there  may  be  hemi-anaesthesia  of  the 
contra -lateral  side  of  the  body.  According  as  the  growth  is 
primarily  intra -pontine  or  extra -pontine  in  origin,  the  affection 
of  cranial  nerves  will  be  primarily  nuclear  or  infra -nuclear  in  type 
and  the  grouping  of  the  symptoms  will  be  slightly  different.  We 
have  already  studied  the  differences  between  a  nuclear  and  an 
infra-nuclear  affection  of  the  sixth  and  seventh  nerves  (see  pp.  139 


452  NERVOUS   DISEASES 

and  152).  Tumours  of  tlie  auditory  nerve  are  relatively  common, 
and  often  bilateral ;  they  ultimately  produce  signs  of  extra -cere- 
bellar growth,  as  we  have  seen  (p.  449). 

The  clinical  picture  of  alternate  paralysis  is  often  masked  by 
the  fact  that  pontine  tumours  rarely  remain  confined  to  one  side, 
but  tend  to  spread  bilaterally.  In  such  cases  we  depend  for  our 
diagnosis  on  the  existence  of  nuclear  or  in^ra -nuclear  paralysis 
of  the  fifth,  sixth,  and  seventh  nerves,  together  with  signs  of 
implication  of  the  motor  or  sensory  tracts  or  of  the  cerebellar 
peduncles. 

Tumours  of  the  Medulla  Oblongata. — In  this  region  the  chief 
diagnostic  feature  is  paralysis,  unilateral  or  bilateral,  of  the  lowest 
cranial  nerves,  from  the  ninth  to  the  twelfth,  producing  disorders  of 
articulation,  deglutition,  &c.,  together  with  signs  of  interruption 
of  the  afferent  or  efferent  tracts  coursing  through  the  medulla. 

Tumours  of  the  Fourth  Ventricle  may  arise  either  from  the 
ependyma,  or  from  the  choroid  plexus,  or  they  may  be  parasitic 
cysts  caused  by  cysticerci.  In  such  ventricular  growths  focal 
symptoms  may  be  absent.  If,  however,  the  lesion  extends  into 
the  dorsal  part  of  the  pons  or  medulla,  or  into  the  cerebellum, 
corresponding  symptoms  develop.  Glycosuria  is  relatively  com- 
mon. We  have  already  referred  to  the  peculiar  form  of  vertigo 
which  occurs  in  cases  of  free  cysticercus  in  the  ventricle  (p.  160). 

Pathological  Diagnosis  of  Intracranial  Growths. — In  any 
given  case  it  may  be  impossible  to  diagnose  with  certainty  the  nature 
of  the  growth,  since  the  symptoms  depend  not  on  the  structure 
but  on  the  anatomical  position  of  the  tumour.  But  if  there  is  a 
history  of  syphilis,  and  still  more  if  the  Wassermann  reaction  is 
positive,  a  gumma  may  be  suspected,  and  in  most  cases  the 
patient  should  be  given  the  benefit  of  energetic  anti-syphilitic 
treatment  for  a  time.  It  must  not  be  forgotten,  however,  that 
even  gummata  sometimes  resist  medicinal  treatment,  and  it  may 
be  necessary  to  remove  a  cerebral  syphiloma  by  operation. 
Syphilitic  lesions  of  the  central  nervous  system  are  usually 
associated  with  an  excess  of  lymphocytes  in  the  cerebro-spinal  fluid  ; 
a  normal  fluid  would,  therefore,  be  against  a  diagnosis  of  syphiloma. 


INTRA-CRANIAL    TUMOURS  453 

But  an  excess  of  lymphocytes  occurs  not  only  in  tuberculous 
tumours,  but  even  in  true  neoplasms.  A  sudden  apoplecti- 
form aggravation  of  the  symptoms  is  suggestive  either  of  glioma 
or  of  aneurism,  gliomata  from  their  loose  texture  and  high 
vascularity  being  particularly  liable  to  spontaneous  haemorrhages. 
Aneurisms  sometimes,  and  arterio -venous  aneurisms  more  often, 
may  be  accompanied  by  pulsating  bruits  ;  these  may  not  only  be 
perceptible  by  the  patient  but  can  sometimes  be  auscultated  by 
the  physician.  Cerebral  abscesses  are  mostly  secondary  to  local 
infection,  especially  from  the  middle  ear  or  other  accessory  air- 
sinuses  (frontal,  ethmoidal,  or  sphenoidal),  or  they  may  follow 
compound  fractures  of  the  skull ;  less  commonly  we  find  metastatic 
abscesses  [e.g.  in  pyaemia  and  in  some  cases  of  bronchectasis,  hepatic 
abscess,  &c.),  without  Iccal  infection  in  the  head.  Tuberculous 
growths  are  specially  common  in  the  pons  and  cerebellum,  and 
the  existence  of  tuberculous  disease  of  the  lungs,  abdominal  viscera, 
or  elsewhere,  would  tend  to  suggest  a  similar  cause  for  the  intra- 
cranial mischief,  particularly  if  the  patient  be  a  child  or  young 
adult.  Calmette's  ophthalmo-reaction  by  inoculating  the  conjunc- 
tiva, or  Von  Pirquet^s  cuti-reaction  by  inoculating  the  skin  with 
a  solution  of  tuberculin,  or  an  estimation  of  the  opsonic  reaction 
of  the  blood  to  tubercle,  are  sometimes  of  value  in  such  cases. 
Symptoms  of  cerebral  tumour  supervening  in  a  patient  who  has 
already  had  a  malignant  tumour  elsewhere  in  the  body  suggest 
that  the  cerebral  mischief  is  metastatic  in  nature.  In  such  cases 
a  curative  operation  is  out  of  the  question,  since  it  is  probable  that 
other  tumours  will  be  present,  besides  the  one  which  has  been 
diagnosed. 

Finally,  we  have  to  bear  in  mind  certain  cases  of  pseudo-tumor 
cerebri,  which  may  be  divided  into  four  groups  : — (1)  Cases  which 
after  showing  the  classical  signs  of  brain  tumour  recover  completely 
or  in  which  an  autopsy  shows  no  lesion  capable  of  accounting  for 
the  symptoms.  (2)  Cases  of  acute  hydrocephalus,  serous  meningitis 
of  the  ventricles  (ependymitis)  without  discoverable  cause  and 
relieved  by  thecal  puncture.  (3)  Localised  ependymitis  of  the 
Sylvian  aqueduct,  producing  blocking  of  this  canal  with  enormous 


454  NERVOUS    DISEASES 

distension  of  the  ventricles.  (4)  Extensive  and  acute  softenings, 
with  headache,  choked  discs,  and  hyper-tension  of  the  cerebro- 
spinal fluid . 

As  a  rule,  however,  pseudo-tumor  is  more  rapid  in  its  evolution, 
and  the  optic  and  ocular  phenomena  appear  early  and  soon  attain 
a  maximum. 


INDEX 


Abadie's  sign  of  tabes,  194,  204 
Abdomen — 

motor     points     of     wall     (Erb's 
diagram),  392 
Abdominal     reflex — significance     of 

absence,  317 
Abdominal  sympathetic,  diseases  of — 
pigmentary  changes,  cutaneous, 

347 
visceral  disorders,  345,  346 
Abductor  palsy  of  larynx,  166,  167 
Abscesses  of  brain,  453 
aphasia  from,  98 
cerebro-spinal  fluid  in,  412 
fits  due  to  cortical,  73 
headache  due  to,  175 
Absinthe-poisoning,    coma   and    con- 
vulsions from,  70 
"  Acetone  "  breath,  63 
Achilles- jerk,  325 
Achromatopsia,  123 
Acromegaly,  123,  292,  447 
Aero  parsesthesia,  348 
Active  muscle-sensation,  190 
Addison's  disease,  347 
Adductor  paralysis  of  larynx,  167,  168 
Adiposis  dolorosa  (Dercum's  disease), 

291 
Adiposo -genital  degeneration,  447 
Aerophagy,  385 
Afferent  impulses,  2,  12,    13    et  seq.  ; 

path  of,  13,  15;  diagrams,  14,  17 
Ageusia,  144 
Agoraphobia,  360 
Agraphia,  97,  103,  104 
Aichmophobia,  360 
Air-swallowing,  385 
Akinesia  algera,  189 
Albinism,  nystagmus  in,  133 
Albumin,     excess    in     cerebro-spinal 

fluid,  408 
Albuminuria,  orthostatic,  347 
Albuminuric  retinitis,  diagnostic  sig- 
nificance, 70 
Alcoholism — 

amblyopia  of,  123 

articulation  in,  112 

ataxia,  264 

coma  and  convulsions,  61,  70 

facial  paralysis  in,  155 

factor  in  nervous  disease,  51,  54 

gait  in,  285 


Alcoholism  (continued) — 
insomnia  in,  431 
men  and  women,  effects  in,  51,  52 
neuritis     from,      52  ;       multiple 

neuritis  from,  205,  233 
paralysis,  155 
Quinquaud's  sign,  84 
toxic  vertigo,  161 
tremor,  84 
Alexia,  102  et  seq. 
Allocheiria,  193,  196,  374-5 
Alopecia,  305 
Alternate     paralysis,      209,     217-18, 

451 
Amaurosis,  hysterical,  373-375 
Amaurotic  family  idiocy,  125 
Amblyopia,  crossed,  37,  38 

inhj^steria,  123,  372;  in  tumours, 
442 
Amblyopia,  tobacco,  120,  122,  125 
Ambulatory  automatism,  70,  378 
Ammonium  sulphate  test   for  globvi- 

lin,  409 
Amnesia  retrogade,  55 
Amyotonia  congenita,  279 
Amyotrophic  lateral  sclerosis,  80,  111, 

220,  225,  326 
Anaemia — 

cerebral,    causing   vertigo.    159  ; 

and  sleep,  423,  425 
headache  of,  176,  177 
mydriasis  in,  128 
optic  neuritis  in,  125 
primary    thrombosis   of    sinuses 

in,  59,  60 
tinnitiis  in,  158 
Anaesthesia — 

auto-exploration    of    sensibility, 

193 
crossed,  16 
cutaneous,  35,  191-8 
dissociated,  196,  202-3 
hemi- anaesthesia.     See  that  title 
hysterical,   197-9,202,  367-373; 
mode  of   disappearance,    372; 
diagrams,  369-373 
mapping  of  areas,  191-3 
para-anaesthesia,  201 
in  peripheral  neuritis,  IS 8 
spinal,  after-effects,  422  ;  contra- 
indicated,  421';    mode    of   in- 
ducing, 418-422 


456 


INDEX 


Anaesthesia  (continued) — 
of  spinal  lesions,  201 
incomplete,  202 
tabetic,  203 
tactile,  195,  196 
thermo-,  196,  202 
in  tubercula  dolorosa,  188 
universal,  of  hysteria,  198 
Ansesthetics,    delayed    poisoning  bv, 
63 
spinal,     examples    of    sokitions, 
418  note 
Anal  reflex — 

internal,  330,  332 
superficial,  317,  318,  320 
Analgesia,  196,  204 

in  tabes,  194,  204 
Anarthria,  articulative,  97,  105 
Aneurisms,  intra-cranial,  157,  453 
pulsating  sounds  in,  157,  453 
Angina  pectoris,  182,  347 
Angio-neuroses,  51,  347-353 
Angio-spastic  hemiplegia,  252 
Anidrosis,  localised,  344,  353 
Ankle-clonus,  213,  282,  327  ;  spurious, 

213,  328,  383 
Ankle-jerk,  321,  325 
Anorexia  nervosa,  291,  385 
Anosmia,  49,  73,  118,  146^;    in  brain 

tumours,  441 
Anterior  cornua,  cells  of,  2,  3,  27,  80 
deep  reflexes,  loss  of,  326 
lesions,  80,  222,  224 
motor  palsy  in,  222,  223 
motor  tract  through,  2,  13,  27 
posture    in    muscular    paralysis 
from,  267 
Anterior    nerve    roots.      See     Spinal 

Nerves — Roots 
Anterior       polio-myelitis       (infantile 
paralysis) — 
acute,  222 
chronic,  224 

loss  of  deep  reflexes  in,  326 
Anterior  transverse  gyrus  of  Heschl, 

39,  40,  96 
Antrum  of  Highmore,  empyema  of, 

119 
Anuria,  hvsterical,  386 
Aphasia,  95,  108 

auditory,  97,  100,  442 

causation,  105 

cortical      centres      involved      in 

(diagrams),   101,  103,   104 
dysarthria  distinct  from,  109 
functional,  or  temporary,  99 
hysterical,  104 
lachrymosis  in,  51 
Marie's  views,  105 
motor,  97,  101,  105,  440 
sensory,  9"^,  97,  100-104,  105,  106 
scheme  for  investigation  of,  99 
total,  105 
visual.     See  that  title 


Aphemia,  97 

Aphonia,       hysterical,        116,       364, 

388 
Apoplexy,  diagnosis  of,  57,  408 
Appendicitis,  pseudo-,  386 
Apraxia,  106 

in  callosal  tumour,  445 
in    relation   to    corpus    callosum 
(diagram),  107 
Arachnoidal  sac,  403 
Argyll-Robertson  pupil,  127,  129 
Arm,  cerebral  paralysis  of,  9,  11 

sensory  fibres  from,  19 
Arsenical  poisoning — 

cutaneous  affections,  303 
multiple  neuritis  due  to,  233 
Arteries — 

cerebellar,  44 
cerebral,  41-45 
diseases  of,  58 
of  spinal  cord,  45 
Arthropathies,  308-315 
Articulation,  disorders  of,  109-117 
alcoholic,  112 
ataxi(;,  112 
deaf-mutes,  116 
functional    cortical    distvirbance, 

115 
general  paralj'sis  of  insane,  113 
hysterical,  116,  364 
idioglossia,  117 

infra-nuclear  and  nuclear  affec- 
tions of,  110 
lalling  and  lisping,  117 
paralytic,  110-116  et  seq. 
supra-nuclear  affections  of,  112     - 
tests  for,  109 
tics  of,  116 
Articulation      distinguished      from 

speech,  109 
Asphyxial  convulsions,  70,  74 
Associated  movements,  88,  214 
Astasia-abasia,  283,  382,  388 
Astereognosis,  195  ;   of  brain  tumour, 

443 
Asthenic  bulbar  paralysis,  248 
Asthma,  dyspnoea  of,  348 
Astigmatism,  headache  of,  175 
Asynergia,  2',  263,  448,  450 
Ataxia.       See    Inco-ordination     and 

Tabes 
Athetosis,   49,87,  265;    double,  113; 

figures  of  case,  88 
Atopognosis,  193 

Atrophy,  acute  yellow,  coma  of,  64 
Atrophy,    muscular,     208,     236-238, 
399 ;    in   hysteria,    247 ;    Werdnig- 
Hoffmann  type,  225 
Auditives  and  visuals,  98 
Auditory  aphasia.  97,  100,  105 
of  brain  tumour,  442 
cortical  and  sub-cortical,  100-101 
Auditory  centre,  39,  96-100,  105 
Auditory  gyrus  (Flechsig),  39,  96 


INDEX 


457 


Auditory   nerve,    affections   of,    and 

tests,    156 
Auditory  path,  39 
Auditory  word  centre,  97-102 
Aura  preceding  epilepsy,   66 
Auriculo-ventricular     muscle-bundle 

of  Kent  and  His,  75 
Auto-exploration  of  cutaneous  sensa- 
tion, 193 
Automatism,   3 

ambulatory,  70 
hysterica], '378 
post-epileptic,  69 
Avellis's  syndrome,  105 

Babinski's   combined  flexion  of  hip 
and   trunk,  212;    extensor  plantar 
reflex,  318 
Barany's  thermic  nystagmus,  134 
Basilar  artery,  41 

Bed-sores,   50,   235,    298 ;    non-occur- 
rence in  hysteria,  38G 
Bell's  paralysis,  149,  231,  402 
Benedikt's  syndrome,  86,  217,  446 
Beri-beri,  233 
Biceps  muscle,  34 

atrophy    from    anterior    cornual 

lesion,  268 
reflex,  321 
Biernacld's  sign  in  tabetic  anajsthesia, 

204 
Bi- temporal  hemianopia,  123 
Bladder — 

disorders  due  to  lesions  of  cord 

or  rauda  equina,  330 
dribbling  from,  332 
in  hysteria,  384 
innervation,  331-2 
reflex    centres    for    contraction. 
331,  332 
"  Bleeding  diseases,"  58 
Blepharospasm,  93,  379 
Blindness,  in  amaurotic  family  idiocy, 
125 
hysterical,  373 
lesions  causing,  38 
Blood-pressure,  in  coma,  56 

effect  of  pituitary  secretion  on, 

26 
intra-cranial ,  408 
Blood-vessels — 

angio-neuroses  affecting,  347-8 
cervical  -  sympathetic    flbres   to, 
334 
Blue  oedema,  hysterical,  387 
Bones — - 

atrophic    changes    in    paralysis, 

306-309 
brittleness  in  disease,  308-309 
convulsions     due    to    injury    of 

cranial,  73 
sensory  fibres  from,  1 8 
trophic  changes  in,  306-13 
Borborygmi,  385 


Bracliial  neuralgia,  184 
Brachial  paraplegia,  209 
Brachial  plexus,  paralysis  of,  341 
Brain — 

abscess    of,    73,    98,    175,    412, 
453 

anaemia  of,    159,  425 

anatomy  and  physiology  of ,  1-21 

arterial  supply,  41-45 

base,  arterial  supply,  41,  43 

circulation      in,      arterial,      41 ; 
venous,  45 

concussion     of,     55 ;     headache 
after,  177 

cortex,  histology  of,  5-6 

haemorrhage.     See  under  Hsemo  - 
rhage,  cerebral 

hypersemia  of,  159 

lesions,  palsies  due  to,  9-11,  219; 
rhythmic  tremor  in,  86 

localisation  of  function,  4-9 

membranes  innervation,  173 

motor  areas,  localisation  of,  4 

sensory  tracts  in,  17 

in  sleep,  423-433 

traumatic       haemorrhage      with 
"  compression,"  59 

tumours.      See    under   Tumours, 
intra-cranial 

venous  supply,  45-47 
Breathing — 

in  cerebral  concussion,  55 

in  cerebral  haemorrhage,  56 

in  diabetic  coma,  63 

in  hysterical  trance,  64 
"  Breites  Bein,"  Heilbronner's,  273 
Brissaud's  reflex,  318 
Broca,  cortical  centre  of,  43,  97,  105 
Brown-Sequard     paralvsis,      11,     19, 
195,  196,  202,  220 

diagram  of  symptoms,  19 
Brudzinski's  signs  of  meningitis,  60 
Bvilbar  palsy  (glosso-labial-laryngeal 
paralysis).   111 

articulation  in.  111 

lachrymosis  in,  51 

mixed  electrical  reactions  in,  401 

pseudo-,  113,  219 

tongue  tremors  of,  80 
Bulbar  phenomena  in  Meniere's  dis 

ease,  161 
Bulbo-cavernosus  reflex,  317,  320 

C.\isso^  disease,  186 

Calcarine    fissure,  37;  lesions  of,  125, 

443 
Calmette's  ophthalmo-reaction,  453 
Capsule,  internal,  anatomy  of,  6-8 

motor  fibres  of,  6 
Carcinoma,  434;   coma  of,  64 
Caries  (dental) — 

headache  due  to,  175 

neuralgia  due  to,  180 
Caries,  spinal,  187 


458 


INDEX 


Carotids,  internal,  41 
Carpo-metacarpal  reflex,  321 
Case-taking,  method,  of,  48-54 
Cataract,  cortical,  120 

and  tetany  of  gastric  origin,  77 
Catalepsy,  68,  377 
Catheterisation,  rigor  following,  79 
Cauda  equina— 

lesions  of,  234-236 

anal  ancssthesia  from,  333 
bladder  trouble  in,  331 
bulbo-cavernosus  reflex,  loss 

of,  320 
gait  in,  287 

motor  paralysis  due  to,  234 
relations  with  vertebral  column 

(diagram),  404 
roots  of,  403 
Caudate  nucleus  (diagrams),  7,  8 
Cavernous  Sinus,  thrombosis  of,  46 
Cells,  nerve,  physiology  of,  1 
Central  scotomata,  121 

for  colours  in  tobacco  amblyopia, 

119,  122 
in  retrobulbar  neuritis,  126 
Cerebellar  tract,  direct,  21-25 
Cerebellum — 

anatomyand  physiology  of,  21-26 

arterial  supply,  44 

ascending    tracts    in    connection 

with,  29 
ataxia,  or  asynergia,  263 
connections  of  (diagram),  23 
cortex,  22;    low  excitability  of, 

24  ;  motor  centres  in,  23-25 
equilibration,  co-ordinating 

centre  for,  24,  158 
functions,  24-26 
indirect   action   on   spinal    cord, 

24-25 
intoxication  of,  112,  264 
lesions  of — 

ataxia  due  to,  258,  260-264 
attitude  in  (fig.);  286 
dysdiadocho-kinesia,  448 
fits  due  to,  77,  448,  450 
forced  rotatory  movements, 

450 
gait  in,  285 
motor  effects,  24 
nystagmus  in,  134 
skew  deviation  of  eyes  from, 

138 
vertigo  in.  158 
nuclei  within,  22 
peduncles  of,  21-24,  158 
section  through  (diagram),  22 
tracts  leading  to  and  from,  23 
tumours  of,    160,  178,  285,  435- 
438,  448 
Cerebral  ataxia,  264 
Cerebral  sinuses,  thrombosis  of,  46 
Cerebral.      See  also  under  Abscesses, 
Brain,  Hsemorrhage,  and  Tumours 


Cerebro-spinal  fluid,  51,  403-422 
cryoscopy  of,  408 
cyto-diagnosis  of,  411 
diagnostic     significance    of,     48, 

71,  407-422 
examination  of,  389-412 
Ivmphocytosis  of,   71,    181,   254, 
"  298,  411 
parasites  in,  411 
pathological  conditions — 

bacteriological    characters, 

409 
cellular  changes,  187-188 
chemical  characters,  408 
microscopical  characters, 410 
physical  characters,  407 
punctiuring  for,  403-407 
therapeutic  applications  of,  415- 

418 
tumour-cells  in,  41 1 
Cervical  plexus,  29,  30,  145 
Cervical  region  of  cord — 

lesions  in,  128,  181,  209,  218 
muscular  localisation  in,  34 
Cervical  sympathetic — ■ 

course  and  distribution,  126,  142, 

170,  334-336 
in  diagnosis,  51 
excision  of,  344 
lesions,  336 
oculo-pupillary  fibres,  course  of 

(diagram),  336 
paralysis  of — 

from    brachial   plexus    rup- 
ture, 341 
from  tumour,  339 
symptoms  of,  337-340 
stimulation  of,  clinical,  338,  345 
sweat-fibres  supplied  by,  343 
Charcot's  "  grande  hysteric,"  377 
"  migraine    ophtalmoplegique," 

140 
tabetic  joints,  309 
Charcot     and     Marie's     progressive 

neuritic  amyotrophy,  228 
Chemosis,  47 

Chloral  poisoning,  tremor  in,  84 
Chloroma,    cerebro-spinal    fluid    in, 

412 
Cholin  in  cerebro-spinal  fluid,  409 
Chorda  tympani,  143,  148,  152,  155 
Chorea,  49,  86,  87 

articulative  defects  in,  115 
ataxia  in,  264 
gait  in,  288 
Huntington's,  87 
hyoscine,  87 
rheumatic,  87 
sores  in,  298-299 
tic,  distinct  from,  91 
Choroid  artery,  anterior,  42 
Choroiditis,  49,  125 
Chvostek's  sign  of  tetany,  77 
Cigarette  smoking,  toxic  effects  of,  84 


INDEX 


-  459 


Ciliar J' ganglion,  126-128,  139 

degeneration  (diagram),  127 
Ciliary  muscle,  inner\'ation  (diagram), 

126-127 
Ciliary  nerves,  128 
Cilio-spinal  centra  (diagram),  336 

reflex,  51,  330,  338,  340 
Circumflex  nerve,  29-30 
Circumvallate  papillse,  143,  1J5 
"  Claudication    intermittente,"     186, 

188,  251,  351 
Claustrophobia,  360 
Clavus  hystericus,  167,  365 
Claw  hand,  270 
Clonus,  327-29 

pseudo- clonus,  327,  384 
Cocaine — 

injection    by    lumbar    puncture, 
418 

ocular  phenomena  produced  by, 
128,  341,  345 
Coccygodynia,  184 
Cochlear  fibres,  auditory  ner  ve,  40, 156 
Cochlear  and  vestibular  nerves,  con- 
nections (diagram),  40 
Colitis,  muco-membranous,  347 
Colovir  blindness,  121 
Colour    vision,    tests    for,     121  ;      in 

hysteria,  373 
Coma,  55-64 

of  acute  yellow  atrophy,  59 

of  alcoholic  intoxication,  61 

bladder  trouble  in,  332 

carcinomatosum,  64 

from  cerebral  concussion,  55 

from  cerebral  hsemorrhage,  57 

from  cerebral  meningitis,  60 

diabetic,  63 

diagnosis  and  causation,  56 

hysterical  trance  and,  64 

malarial,  64 

of  opium  poisoning,  61 

of  pontine  haemorrhage,  59 

post-epileptic,  62 

and  sleep,  426 

in  sunstroke,  63 

in  Stokes -Adams  syndrome,  62 

in  thrombosis  of  cerebral  sinuses, 
59 

toxsemic,  56 

ursemic,  62 
Concussion  of  brain,  55,  177 
Congenital  ptosis,  140 
Conjugate  deviation,  9,  138,  440 
Conjunctiva — 

anaesthesia,  in  fifth    nerve    par 
alysis,  145 

conjunctival  reflex,  150,  317 

nerve-supply,  142-3 
Consanguinity  of  parents,  49 
Consciousness,  double,  359,  377 
Consonants,  articulation  of,  112,  117 
Constipation — 

occipital  headache  of,  177 


ConstijDation  (contin uexl) — 

toxic  vertigo  from,  160-1 
Constrictor  urethrae,  332 
Contractures,  hysterical,  383 
Conus  meduUaris,  235 
Convulsions — 

generalised  epileptiform,  436 
infantile,  73 
strychnine,  75 
See  also  Fits 
Coprolalia,  91 
Coprophobia,  360 
Corona  radiata,  6 
Corpora  dentata,  21 
Corpus  callosum,  relation  to  apraxia 

(diagram),  107 
Corpus  quadrigeminum,  22,  37,  446 
Corpus  striatum  syndrome,  294 
Cortex — 

arterial  supply  of,  41 
cerebral,  diagrams  of,  5 
lesionS: — 

anaesthesia  due  to,  199-205 
fits  in,  65,  71-78 
motor  palsy  from,  215-221 
motor,  inco-ordination  in,  264 

lesions  of,  9 
venous  supply,  45 
Cortical  cells  in  sleep,  424 
Cortical  centres — 

auditory,  39-40,  96-100 

half- vision,  32,     37,     103,     124, 

421 
of  hunger  and  thirst,  39 
motor,  4-6 
olfactory,  36,  118 
sensory,  3 

of  speech,  96-97  ;   diagrams,  96, 
98  ;   mal-development,  116-7 
of  taste,  39 
of  vision,  37,  104 
of  writing,  97 
Cortical  localisation  (diagrams),  5 
Cortico-spinal  motor  neurone,  lesions. 

See  Motor  Paralyses 
Cortico-spinal  tracts,  11-13 
Cough,  hysterical,  388 
Craft  palsies  and  cramps,  253 
Cranial  bones,  headache  from  affec- 
tions of,  175 
inspection  of,  52 
Cranial  nerves — 

Abducens  (Sixth),  117;  lesions 
of,  10,  126;  paralysis  of,  47, 
137,  438 
Aviditory  (Eighth),  156-163  ; 
cochlear  division,  39,  156  ; 
diagrams  of,  119,  120;  ves- 
tibular, 156 
Facial  (Seventh),  148-155 

lesions    at    different    levels, 

148-155 
motor  root,   149-152 
secretory   and   taste   fibres, 


460 


INDEX 


Cranial  nerves — Facial  {continued) — 
course  of  (diagrams),  39, 

142,  149,  151,  155 
sensory  root,  39,  155 

Functions  of,  49-50 
Glosso-pharyngeal    (Ninth),     39, 

143,  163 

course  of   taste-fibres    (dia- 
gram), 142-3,  155 
Hypoglossal  (Twelfth),  170-172, 
335 
paralysis,    170  ;     unilateral, 
110 
Nervus  intermedins  of  Wrisberg, 

39,  155 
Oculo-motorius  (Third)  126 

paralysis      of,      131-2,   135, 

144,  217 

Olfactory  (First),  36,  118-119 
Optic  (Second),  37,  119 
Patheticus   (Fourth),    126  ;    par- 
alysis, of,  46,   136 
Recurrent    laryngeal,    Linilateral 

paralysis  of,  111 
Short  ciliary  nerves,  128 
Spinal  accessory  (Eleventh),  1 67  ; 
paralysis  (diagrams),  167-lfi9  ; 
and  of  hypoglossal,  170-171 
Trigeminal      (Fifth),       141-147, 
cutaneous  supply  to  head  (dia- 
gram), 141 
distribution,  141-143 
incidence     of      rodent     ulcers 

over,  299-300 
lingual  branch  of,  143-144 
ophthalmic      division,      lesion 

of,  337 
pains  in  region  of,  179-180 
paralysis  of,  144,  145 
sensory  root  of,  16,  39 
sweat      areas      corresponding 

with  area  of,  353 
taste    fibres,    course    of    (dia- 
gram), 142 
Vagus  or  Pneumogastric  (Tenth), 
164 
paralysis,  166-168 
Vidian  nerve,  142 
Cremasteric  reflex,  317,  320 
Crimes,  in  post-epileptic  automatism, 

69 
Crossed  amblvopia,  37.  38,  123 
in  hysteria,  123,  372 
in  tumours,  442 
Crossed  anaesthesia,  16 
Crossed  hemi-ansesthesia,  18,  201 
Crossed  paralysis,  9-10,  50,  209,  451 
Crus  cerebri — 

lesions  of,  10,  446 

motor  palsy  due  to,  217 
tegmental  region,  86 
Cryoscopic  examination,  408 
Cuneate    lobule,    visual    half-centres 
in,  lesions,  125 


Cutaneous  anaesthesia  in  hysteria,  368 
Cutaneous  sensibility,  14,  15,  191-193 

loss  of,  204 

recovery  of,  230 
Cyanosis  in  chronic  hemiplegia,  352 

in  erythromelalgia,  350 

in  Raynaud's  disease,  348 
Cysticercus  in  Fourth  Ventricle,  diag- 
nosis, 160 
Cy  to -diagnosis,  411-415 

Dahtos  reflex,  333,  419 

Deaf-mutes,  116-117 

Deafness,  152,  156-157,  162-163,  446 

due  to  drugs,  158 
Decubitus,  acute,  298 
Defsecation,  234,  316,  333 
Degeneration,  ascending,  29 

descending,  27 

of  spinal   cord,    combined,    2C0, 
329 

Wallerian,  29 
Deiters'  nucleus,  21-24 

focal  lesion  of,  163 
Delirium,  49 
Delirium  tremens,  52,  84 
Deltoid,  atrophy  of  (diagram),  224—6, 
229 

paralysis  from   anterior   cornual 
lesion,  268 

paralysis  of,  from  lesion  of  cir- 
cumflex, 30 
Dementia,  bed-sores  in,  298 
Dercum's  disease  (Adiposis  dolorosa), 

291 
Dermatomes,  33 
Dermographism  (diagram),  136,  352; 

in  hysteria,  387 
Diabetes — 

breath  in,  63 

coma  of,  63 

insipidus,  347 

multiple  neuritis  due  to,  233 

optic  neuritis  in,  125 

perforating  ulcers  in,  295 

bilateral,  tic  douloureux,  in,  179 
Diadochokinesia,  448 
Diaphragm,  myoclonus  of,  81 
Diarrhoea,  hysterical,  386 

paroxysmal,  of  Addison's  disease, 
347 
Dilator  pupillse,  127,  142,  335 
Diphtheria,  neuritis  after,  130,  233 
Diplegia,  87,  209,  219 

causes  of,  9 

definition  of,  209 

spastic,  282 
Diplococcvis  intra- cellularis,  409 
Diplopia,  136 

false  image,  position  of,  131,  136 

gait  in,  285 

monocular  (hysterical),  376 

ocular  vertigo  with,  161 

tests  for,  131-132 


INDEX 


461 


Dipsomania,  360.    See  also  Alcoholism 
Disseminated  sclerosis — 

absence  of  abdominal  reflex  in, 
317 

ataxia  in,  260,  285 

cholin  in  cerebro-spinal  fluid  in, 
409 

clonus  in,  329 

emotional  state  in,  51 

erythromelalgia  a    symptomi  in, 
350 

motor  paraplegia  due  to,  220 

nystagmus  in,  133 

optic  atrophy  in,  126,  130 

staccato  speech  in,  114 

transient  paralysis  in,  256 

vertigo  in,  160 
Disuse,  atrophy  from,  246,  383 
Dorsal  longitudinal  bundle,  13 
Double  consciousness,  359,  377 
Drop-foot    and    drop-wrist    in    peri- 
pheral neuritis,  205,  233 
Drowsiness,  49,  426-428 

hypnotic,  428 

pathological,  426-428 

toxic,  431 
Dumbness — 

of  deaf-mutes,  116 

of  imbeciles,  116 
Dyssesthesige,  173 
Dysarthria    (see    also    Articulation — 

defects),  109,  112-3,  257 
Dysbasia  angio-sclerotica,  251 
Dysdiadochokinesia,  448 
Dysphagia,  hysterical,  385 
Dystrophy,  muscular.    See  Myopathy 

Eak,  auditory  fibres  of,  39 

disorders — gait     in,      158,      161, 
285 ;  herpes  of  external  audi- 
tory    canal,    148,     155,     297; 
otitis    media.     See    that   title ; 
vertigo  from,  156,  161 
inner,     afferent     impulses     from 
semi-circular  canals,  15S 
Echolalia,  91 
Ectopia  pupillse,  127-9 
Electricity — 

abnormal  reactions,  399-400 
clinical  application  of,  391-8 
faradic  reactions,  390,  397 
galvanic  reactions,  398 
reactions  of  degeneration,  400-2 
Electro-diagnosis,  377-383 

prognosis,  384 
Elephantiasis  nervorum,  303 
Embolism,  41,  44,  45-7,  98, 
Emotional  states,  5 1 
Endolymph,  159,  162 
Enophthalmos,  51,  337,  339,  343 
Enteric  fever,  absence  of  abdominal 
reflex  in,    317;     "coma-vigil"   of, 
64  ;    headache  of,  176 
Enuresis,  332 


Epicritic    cutaneous   sensibility,    15  ; 
loss    of,     204  ;     recovery    of,     14, 

230 
Epigastric  reflex,  317 
Epilepsy,  66-74 

bilateral  excision  of  cervical 
sympathetic  for,  344 

chronic,  posture  and  gait  in,  289 

distinguished  from  hysteria, 
66-9;  and  Meniere's  disease, 
163 

infantile,  73 

Jacksonian,  65,  71-3,  200,  438- 
440 

major,  or  "  grand  mal,"  68,  70 

masked  or  larval,  70 

minor  or  "petit  mal,"  65,  69, 
255 

post-epileptic  automatism,  69  ; 
coma,  62 

preixionitorj?  syinptoms,  66 

sudden  falling,  255 

"  true,"  70 
Epileptiform  fits,  60,  71,  74,  78 

in  alcoholics,  70 

aphasia  following,  99 

in  cerebellar  disease,  77 

cerebral,  classification  of,  65 

deep  reflexes,  abolition  of,  327 

in  general  paralysis  of  insane,  71 

headache  following,  177 

in  intra-cranial  tumours,  72,  440 

Jacksonian,  71,  200,  439 

myoclonus  allied  with,  81 

in  psychasthenia,  71 

sensory,  73 

in  Stokes-Adanas  syndrome,  75 

toxic,  70 

vertigo,  the  aura  of,  160 
Epistaxis,  46,  176 
Equilibration — 

afferent  fibres  for,  19 

centre  for,  24,  158 

impulses,  24 

nerve  of,  156 
Erb— 

juvenile  atrophic  myopathy,  243 

motor  points,  391-7 

tetany,  sign  of,  77 
Ereuthophobia,  360 
Erythromelalgia,  51,  188,  350 
Eulenberg's    disease     (Paramyotonia 

congenita),  250 
Eunuchism,  pituitary,  447 
Eustachian  tube,  obstruction  causing 

vertigo,  158 
Exophthalmic  goitre — 

alopecia  in,  305 

cramp  in,  254 

cutaneovis  pigmentation  in,  347 

dermographism  in,  352 

von  Graefe's  sign  of,  345 

intestinal  symptoms,  347 

Mcebius's  sign,  135 


462 


INDEX 


Exophthalmic  goitre  (continued) — 

stimulation       of       sympathetic, 

symptoms  due  to,  345 
tremor  in,  83 
Exophthalmos,  51,  227,  345 
Extensors,  paralysis  of,  30 
Eye,  muscles  of — 

innervation  of,  10,  126 
paralysis  of,  47,  131-140,  438,  447 
Eyebrow  in  Third  nerve  paralysis  and 

hysterical  ptosis,  135 
Eyes,  "  conjugate  deviation  "  of,  9 
See  also  under  Optic,  Pupils,  end 
Vision 

Facial  anaesthesia,  lesions  caiising,  16 
Facial  hemi-atrophy,  progressive,  147, 

305-306 
Facial  hemi-spasm,  93,  154 
Facial  motor  points  (Erb's  diagram), 

391 
Facial  muscles,  50  ;  innervation,  140, 

148-151 
Facial  palsy,  149-155 

articulative  difficulty  in,  110 
auditory   nerve   disease     accom- 
panying, 157 
contracture  secondary  to,  154 
lesion  of  Sixth  nucleus,  associated 
with,  130 
Facio  -  scapulo  -  humeral     myopathy, 

110,  155,  238,  242,  244 
Faeces,  incontinence  of,  333 
Fallopian  aqueduct,  143,  148  ;  lesions, 

152 
Family  gangrene,  350,  351 
history,  49 
hypertrophic  interstitial  neuritis, 

226-227 
periodic  paralysis,  253,  326,  351, 
400 
Faradic  electricity,  390 
Fatigvie — 

temporary  ataxia  of,  264 
tremor  of  muscular,  83 
Fevers,  bladder  trouble  in,  332 
Fibrillary  movements,  49,  80 
Fillet,  39  ;  degeneration,  29  ;  superior 

decussation  of,  19 
Fissures — 

calcarine,  37 
diagram,  8 
lesions,  126,  442-3 
parieto-occipital,  42 
Rolandic,  4,  6.  16,  19 
Sylvian,  4,  8,  39,  41,  96 
Fits,  49,  65-78 

cerebellar,  7"^,  450 

cerebral,  65 

classification,  65 

cortical  lesions  and,  71-73 

epileptiform.     See  that  title 

hysterical.     See  binder  Hysteria 

infantile,  73 


Fits  {continued) — 

Jacksonian.     See  that  title 

scheme  of  investigation,  66 

strychnine  causing,  75 

in  sub-cortical  tumours,  71-73 
Flaccid  paralysis,  28,  213,  380,  383  ; 

fig.,  362 
Flechsig's  aiiditory  gyrus,  39 
"Folic  de  pourquoi,"  300 
Foramen — 

of  Key  and  Retzivis,  406 

of  Magendie,  406 
Forced  rotatory  movements,  450 
Formatio  reticularis,  lesions  of,  16 
Formication,  50 

Fractures,  depressed,  fits  due  to,  73 
Fragilitas  ossium,  307-8 
Friedreich's  ataxia,  89,  2C0-2 

articulation  in,  112 

deep  reflexes,  loss  in,  260,  326 

gait  in,  285 

Marie's    ataxia    compared    with, 
263 

nystagmus  in,  134 

spontaneous  movements  in,  89 

tabes  distinguished  from,  261 
Functional     and      Organic     disease, 
boundary     line     between,     52-53, 
355-388  note 
Fundus,pathological  conditions  of,  1 25 

Gait,  267-289 
ataxic,  284 
cerebellar,  263,  285-6 
in  chorea,  288 
of  chronic  epilepsy,  289 
in  cysticercus  of  Fourth  Ventricle. 

160 
in  deformities,  ,289 
high-stepping,  286 
hysterical,  282,  382 
of  paralysis  agitans,  287,  288 
side  (Flankengang),  283 
spastic,  282 
testing,  mode  of,  280 
Galvanic  batteries,  389,  398 
Ganglia.        See     Ciliary,      Gasserian, 

Geniculate,  &c. 
Gangrene — 

family,  351 

hysterical,  387  ;    fig.,  283 
symmetrical  of   Raynavid's   dis- 
ease, 299,  348 
Gasserian    ganglion    (diagram),    127, 
128,  141,  143,  147,  335;  inflamma- 
tion (diagram),  297 
General  paralysis  of  insane — 

Argyll-Roberfcson      phenomenon 

in.  127,  129 
articulation  of,  113 
cerebral  haemorrhage  in,  58 
cerebro -spinal  fluid  in,  254,  409, 

413 
deep  reflexes,  loss  in,  326 


INDEX 


463 


General  paralyis  of  insane  (conf.) — 
epileptiform  fits  in,  ()9,  70 
hemiplegia  in,  252-4 
pupils  in,  127,  129 
tremors,  spontaneous  in,  91,  113 
Geniculate    ganglion,    142,    148-151, 
155 
inflammation  of,  148,  155,  297 
Genital  reflex,  330 
Genu  recurvatum,  278  :    fig.,  275 
Giddiness,    137,    152,    175,  417,    434, 
43(3 
hysterical,  102 
See  also  under  Vertigo. 
Gigantism,  292,  447 
Glaucoma,  162,  344 
Gliomata,  453 
Gloljulin  in  cerebro -spinal  fluid,  tests 

for,  408-9 
Globus  hystericus,  66,  76,  376,  385 
Glosso-labial  hemi-spasm,  276,  382 
Glossy  skin,  50,  294 
Gluteal  reflex,  317 
Glycosuria,  160,  347,  447,  452    . 
Gordon's  paradoxical  flexor  reflex,  319 
Gowers'  tract,  diagram,  &c.,  16-17 
Grasset  and  Gaussel's  test,  212 
Gumma,  intra-cranial,  180,  453 
fits  from,  72 

headache  due  to,  175,  178 
neuralgia  duo  to,  180 
Gustatory  path,  39,  143;  diagram,  142 
Gyrus,  angular — 

arterial  supply,  43 
cortical  lesion,  123,  442 
visual  word  centre,  39,  97,  102 
auditory  (Flechsig's),  39 
Heschl's,  39,  98 

tumoiu:s  of,  442 
lingual,  33 

uncinate,  lesions  of — 
fits  due  to,  72-73 
olfactory      centre,      33;      dis- 
orders of,  118 
tumours  of,  442 


Habit  spasms,  90,  93,  379,  388 
Hsemoglobinuria,  paroyxsmal,  350 
Hsemophilia,  58 
Haemorrhage,  cerebral — 

aphasia  from,  98 

artery  of  (diagram),  41 

blood  pressure  in,  408 

cerebrospinal  fluid  in,  407—409 

in  children,  58 

coma  in,  57 

diagnosis  of,  52,  59,  408 

in  general  paraly  is  of  insane,  58 

Meniere's    disease    distinguished 
from,  162 

spontaneous,  57—59 

tropic  changes  in  nails  in,  306 

vertigo  from,  158-159 


Hsemorrhage  cerebral  (continued) — 
fits  due  to,  73 
hysterical,  386 
pontine,  59 
retinal,  49 
subarachnoid,  407 
Hair — 

blanching  of,  147,  305 
faUing  of,  49 

in  progressive  facial  atrophy,  147 
trophic  changes,  304-305 
Half-vision  centres,  37,  103,  125,  443 
Hallucinations — 
auditory,  157 
olfactory,  118 
pain,  hysterical  hallucinations  of, 

365 
visual,  72,  444 
Hand,  muscles  of,  lesions  of,  270-271 
Haphalgesia,  375 

Head  "  conjugate  deviation  "  of,  9 
Head  injury,  coma  in,  55 
Headaches,  174-179 

angio-neurotic,  178 

gastric,  176 

of    gross    intra-cranial     disease, 

175,  435 
hysterical,  178,  365 
local   (extra-   and  intra-cranial), 

175 
in  Meniere's  disease,  162 
migrainous ,   178 
neurasthenic,  177 
post-epileptic,  177 
reflex,  176 
in  sunstroke,  177 
toxic,  176 
unilateral,  177 
Head-rolling,  86 
Hearing.     See  under  Auditory 
Hemeralopia,  120 
Herai-achromatopsia,  97 
Hemi-ansesthesia,  196,  199 
crossed,  18,  201 
hysterical,  segmental  type,   199, 

290,  368-373 
organic,  199 

capsular  or  thalamic,  9,  86, 

173,  200 
cortical     and     sub-cortical, 

200,  440 
crossed,  201 

lesions     causing    (diagram), 
18,  20,  200,  445 
Hemianopia — 

bi -temporal  in  pituitary  tumours, 

447 
definitions  and  cause,  123 
diagrams,  38,  122 
lesions    producing,    9,    37,    123, 

439,  443-4 
quadrantic,  37-39 
sub  cortical  word-blindness  asso- 
ciated with,  103 


464 


INDEX 


Hemianopia  {continued) — 
varieties  of,  123-126 
Wernicke's  pupillary  reaction  in, 
130,  443 
Hemi-atrophy,  facial,  147,  306 
Hemi crania,  hysterical,  365 
Hemi-hypersesthesia,  hysterical,  365 ; 

thalamic,  196 
Hemi-hypertrophy,  facial  (fig.)>  289- 

290;  viniversar(fig.),  294 
Hemiopic    pupillary    reaction,   Wer- 
nicke's, 130,  443*^ 
Hemi-paraplegia,  50 
Hemiplegia — 

alternate,  209 

angio-spastic,  252 

aphasia  in,  99 

apraxia  in,  106-108 

articulation  after,  113 

ataxia  associated  with,  264-5 

athetosis  following,  87  ;    fig.,  88 

bilateral,  105,  209 

bed-sores  in,  298 J 

bone-changes  in,  306-308 

capsular  lesion  causing,  9-11 

chronic,  308>  312 

combined  flexion  of  hip  and  trunk 

(diagram),  211 
crossed,  209 

definition  and  forms  of,  209 
dolorosa,  174 
gait  in,  281-284 
in  general  paralysis,  254 
Grasset  and  Gaussel's  sign  of,  212 
headache  preceding,  176 
in  head  injury,  57 
hysterical  (functional),  210,  212, 
274-278,  282-284 
abscesses  of  plantar  reflexes, 

321 
anosmia  in,  118 
infantile,  308  ;   figs.,  272,  276 
ipso -lateral,  216 
joint  affections  in  chronic,  312 
lesions    causing,    diagnosis,     60, 

86,  408,  437 
loss  of  certain  reflexes  in,  320-1 
muscular  wasting  in,  247 
pandiculation  in,  88-9 
posture  in,  269-271 
transient,  253 
tumours  causing,  439-446 
visual  fields  in  cases  of  (diagram), 
374 
Hemispasm,  facial,  93 
Hereditary  ataxia,  Friedreich's,  261; 

Marie's,  263 
Herpes,  facial,  148,  155,  297 
Herpes  zoster,  174,  181,  197,  296-298, 

303 
Heschl's  gyrus,  39,  96 

tumours  of,  442 
Hiccough  in  intra-cranial  disease,  437 
Hippus,  129 


Holmgren's  tests  for  colour  vision,  1 20 
Hunger,  cortical  centre  for,  40 
Huntington's  chorea,  87 
Hydrophobia,  76  ;    hysterical,  76 
Hyoscine  chorea,  87 
Hyperacousis,  152 
Hyperajmia,  cerebral,   157,   159,   175, 

178 
Hyperaesthesia,  195-198 

hysterical,  areas  of,  189,  197,  365 
mapping  out  areas  of,  192 
Hyperalgesia,  198,  365 
Hyperidrosis,  localised,  353 
Hypermetropia,  176 
Hyper-pyrexia,  58,  59,  177 
Hyper-trichosis,  300 
Hypertrophic  interstitial  ne  ritis,  227, 

261 
Hypertrophy  of  muscle,  208 
Hypnotic  suggestion,  64,  361-362 
Hypnotic  trance,  64,  361,  377 
Hypo-sesthesia,  196 
Hypoglossal     nerve.       See      Cranial 

Nerves 
Hypoglossal  nucleus,  148,  171 
Hypo-spinal  ganglia,  335 
Hypotonia  of  muscles,  259 
choreic,    87 

tabetic  (diagrams  of  cases),  276- 
278 
Hysteria,  355-388 

age  and  sex,  effect  in,  66,  388 
allocheiria  in,  193 
alternating  personality,  359,  378 
ambulatory  automatism,  378 
anaesthesia.     See     under    Anaes- 
thesia 
ankle-clonus,  spurious,  213,  311, 

383 
aphasia  and,  104 
articulation  in,  116,  364 
ataxia  in,  265 
bio-chemical  changes  underlying, 

52  note 
Charcot's  "  grande  hysteric,"  68, 

377 
in  children,  362,  388 
concentric  contraction  of  visual 

field,  123,  374 
contractures,  273-276 
crossed  amblyopia,  38,  122 
cough  in,  388 
dermographism  in,  387 
double  consciousness  in,  359,  377 
fits  in — ■ 

catalepsy,  68,  377 
classification,  65 
distinguished  from  epileptic 

fits,  66,  376 
post-epileptic,  66,  69,  376 
gait  in,  282,  382 
glosso-labial  hemispasm,  276 
hemiplegia,    distinguished    from 
organic,  210-213,  274-277 


INDEX 


465 


Hysteria  (continued) — 

hych'ophobia  simulated,  76 
hyperajstlietic  areas   in,  189 
inhibition  deficient  in,  361 
joint  pains  in,  314 
major,  65,  68,  377 
minor,  65,  68 
motor  phenomena  in,  376 
muscular  wasting  in,  246 
neurotonic  reaction  in,  399 
organic     disease,      distinguished 

from,  52  note,  355,  388 
pains  of,  189 

paralysis.     S;e  under  Paralysis 
plantar    reflex    in    diagnosis    of, 

319,  321 
postures  in,  273-277 
psychical  symptoms,  361 
ptosis,  136-137 
reflexes  in,  68,  319-321,  384 
respiratory  modifications,  385 
sensory  symptoms  in,  365 
skin  affections  in,  386 
spasms  in,  94 
speech  defects  in,  364 
trance  of,  64,  377 
transient  paralyses  in,  255 
vasomotor  phenomena  in.  384 
visceral  phenomena  in,  384 
Hysterofrenic  and  hysterogenic  areas, 
186,  365-366 

Idiocy,  amaurotic  family,  125 
Idioglossa,  117 
Imperious  acts,  360 
Impulsss,  origin  of,  1,  6 

paths  of,  15,  19,  24 
Inco-ordination  (ataxia),  257-266 

articulative,  107-117 

cerebellar,  263,  450 

due  to  fatigue,  264 

in  hypertrophic  interstitial  neu- 
ritis, 261 

hysterical,  265 

from     lesions      of     rubro-spinal 
tract,  265 

in  new-born  child,  257 

post-febrile,  264 

pre-  and  post-hemiplegic,  264 

sensory  origin  of,  258 

tests  for,  257 

toxic,  264 
Infant,  new-born,  movements  of,  4 
Infantile  convulsions.  73-75 
Infantile  spinal  paralysis  (acute  an- 
terior    poliomyelitis),     222-226, 
307-309 

lesions  causing,  33,  222-225 

loss  of  deep  reflexes  in,  326 

trophic  changes  of  bones  in,  308 
Inguinal    region,     hysterical    tender 

spots  in,  365 
Injuries,  effect  on  nerves,  14-15 

spinal,  symptoms  of,  19 


Insanity,  toxic  varieties  of,  51 
Insomnia,  429-433 

alcoholic,  432 

drugs,  use  of  in,  430,  432 

emotional,  429 

extrinsic,  429 

and  insanity,  432 

intrinsic,  430 

primary  or  nervous,  432 

vascular  causes  of,  430 
Intermittent  hmp,  186,  188,  251,  351 
Internal  capsule — • 

anatomy,  6-8  ;    diagram,  8 

auditory  fibres  of,  42 

lesions  of  ,  9,  138,  199,  216 

motor  fibres,  6 

sensory  fibres,  8-9 

tactile  fibres,  16 

visual  fibres,  9,  37 
"  Interosseal    attitude"     (diagrams), 

287-9 
Intervertebral  ganglion  (ganglion  cell 

of  posterior  root),  28,  29,  296-7 
Intra-cranial    diseases    and    growths, 
57,    71,     160,   173,    175,    434-454. 
See  also  Tumours 
Tntra-cranial  haemorrhage,  57-8 
Intra-cranial    pressure,    57,    71,    175, 
216,  309,  408,  427 

lumbar  puncture  in  relief  of,  415 
InvoKmtary  movements,  79-94 

myokymia,  80 

reflex  spasms,  92 

rigors,  79 

in  tabes,  89 

tremors,  83-86 
Ipso-lateral  pyramidal  tract,  11 
Ischsemic  paralysis,  236 
Jackson's  syndrome,  172 
Jacksonian  fits,  72-73,  200,  439-440 
Jaw  reflex,  321 
"  Jaw- winking,"  141 
Jendrassik's   reinforcement   of   knee- 
jerk,  322-5 
Jews,       amaurotic      family      idiocy 

amongst,  125 
Joints — 

hysterical  pains  in,  314,  365 

trophic  changes  in,  308-315 
Joint-sense,  190,  259  ;  tests  for,  193 

Keratitis,  bacillus  of,  146 

neuro-paralytic,  146 
Kernig's  sign  of  cerebro-spinal  men- 
ingitis, 60,  298,  413 
Kidney  disease — 

arterio -sclerosis  of   chronic,  ver- 
tigo in,  ICO 
cerebral  haemorrhage  in,  58 
floating  kidney,  183 
nephritis,  70,  125,  417 
uraemic  convulsions  of,  70,  417 
Kinaesthetic  sense,  3,  190,  259  ;    test 
for,  194 

2g 


466 


INDEX 


Kleptomania,  360 
Knee-clonus,  311 
Knee-jerk,  68,  322-5 
Korsakow's  psychosis,  51 

Labials  and  labio-dentals,  articula- 
tion of ,  110 
Labyrinth,  disease  of,  156-8,  161 
cerebellar  gait  in,  263 
vertigo  of,  161-3 
Lachrymal  secretion,  paralysis,  145 
Lactation,  tetany  during,  77 
Lalling,  117 

Landouzy-Dajerine     type     of     myo- 
pathy, 111,  238,  242 
Landry's    paralysis,    222,    233,    326, 

410 
Laryngismus  stridulus,  74,  77 
Larynx — ■ 

ataxy  of,  112 
innervation  of,  164-167 
myoclonus  of,  81 
paralysis,  1 64-7  ;  recurrent,  1 65  ; 
unilateral,   164 
Lasegue's  symptom,  382 
Lateral  lobes  of  cerebellum,  21,  77 
Laudanum  poisoning,  61 
Laufenauer's  method    of    reinforcing 

knee-jerk,  324 
Lead   poisoning — 

convulsions  in,  70 

optic  neuritis  in,  125 

palsy  in,   205,   233  ;    absence  of 

sensory  changes  in,  205,  222 
tremor  of,  84 
visceral  symptoms,  347 
Leg,  paralysis  of,  9,  11,  20 
sensory  fibres  from,  19 
Lenticular  nucleus,  tremors  in  lesions 

of,  86 
Lenticular  zone,  lesions  of,  105 
Lenticulo-striate  artery,  41 
Leprosy      arthropathies       of,      309 ; 
maculo-ansesthetic  type,  301 ;   neu- 
ritis of,  295 
Lepto -meningitis,  localised, compared 

with  spinal  tumours,  220 
Leucocytosis  of  cerebro-spinal  fluid, 

409-415 
Leucoderma,  301 
Leukismia,   58  ;     cerebro-spinal  fluid 

in,  412 
Levator   palpebrse    superioris,    inner- 
vation, 126,  336  (diagram),  lesions 
of.  135,  140,  150,  337-8 
Light  reflex.     See  under  Reflexes 
Liinp,    intermittent,    186,     188,    251, 

351 
Lingual   consonants,   articulation   of, 

110 
Lips,  paralysis  of,  170 
Lisping,  117 

Localisation,  cerebral,  4—9 
Lock-jaw,  75 


Locomotor  ataxia.     See  Tabes 
Longitudinal  sinus,  superior,   throm- 
bosis of,  46 
Lordosis  (with  figs.),  238-240 
Lumbago,  184,  235 
Lumbar  puncture,  52,  403-7 
Lumbo-abdominal  neuralgia,  184 
Lumbo-sacral  cord^ 

disease  symptoms  in,  187 
muscular    localisation     in    (dia- 
gram), 34 
Lumbo-sacral    plexus  and  branches, 

29,  81 
Lymphocytosis       of       cerebro-spinal 
fluid,  71,  181,254,  298  note,  ill-5; 
diagnostic  significance,  412-4 

Macropsia,  375 

Main  de  predicateur,  271 

Main  de  singe,  270 

Main  en  griff e,  270 

Malarial  coma,  64 

Malingering,      Mannkopf's     sign     in, 

365^ 
Mammary  neuralgia,  182,  3G5 
Mannkopf's    sign    of    real    hyperses- 

thesia,  365 
Marie's  hereditary  cerebellar  ataxia, 

263 
Masked  epilepsy,  69 
Mastodynia,  182 
Meckel's  ganglion,  142,  143 
Medulla- 
auditory  fibres  in,  39 
cranial  nerves  (diagram),  119 
lesions  of,    11,    200,   217,   262-3, 

336-7,  452 
Meniere's  disease,  implicated  in, 

161 
pupil-dilating  centre  in,  335 
respiratory  centre  in,  4 
sensory    fibres,     coiirse    of,    17  ; 

diagram,  7 
stimulation  of  nuclei  in,  1 
Melancholic      anergia      distinguished 

from  psychasthenia,  358 
Memory,  49;    loss  of,   51,   55;  post- 
epileptic loss  of,  69 
Meniere's   disease    (labyrinthine   ver- 
tigo), 161-3 
Meninges — • 

cerebral,   convulsions   from   hae- 
morrhage in,  75 
pain,  sensitiveness  to,  173 
spinal,  diseases  of,  187,  298 
root  pains  of,  180,  187 
Meningism,  413 
Meningitis — 

basal,  60,  155,  181 
cerebro-spinal  fluid  in,  61,  407- 

415 
fits  due  to,  75 
fluid  pressure  in,  406-7 
headache  in,  175,  178 


INDEX 


467 


Meningitis  (contimird) — 

lepto-,  localised  spinal,  220 
lumbar  punctiiro  for,  415-G 
septic   cerebro-spinal,    298,   409, 

412 
spinal,  root  pains  in,  187 
syphilitic  basal,  155,  180 
tuberculous,    52,    175,   411,   412, 
415 
Menstrual  periods,  headaches  during, 

176 
Mental     functions,     examination     of 

higher,  51 
Meralgia  paraesthetica,   186 
Mercury  poisoning,  tremor  of,  84 
Metameres   and  root  distribution   of 

sensory  and  motor  fibres,  33 
Meteorism,  347,  352 
Meynert's  fibres,  126 
Micropsia,  376 

Micro-sympathetic  ganglia,  335 
Micturition,  331  ;  centres  for,  331-2  : 

in  hysteria,  384 
Middle  ear — 

disease  of,  153,  156,  161 
innervation,  142-3 
Migraine,      178;      ophtalmoplegique, 

140,  179 
Millard-Gubler  syndrome,   11,  218 
Miners'  nystagmus,  134 
Moebius's  sign  in  exophthalmic  goitre, 

135 
Moles,  hairy,  304 
Molluscum  fibrosum,  303 
Monakow's  bundle  (rubro-spinal),  13  ; 

lesions  in,  139,  265,  327,  446 
"Monkey-hand,"  270 
Monocular  diplopia,  376 
Monoplegia,  9-11,  50.  209;  causes  of, 
9;  definition,  209 ;  hysterical,  379- 
382 
Morvan's  disease,  203,  296 
Motor  act,  reflex,  2  ;  voluntary,  3 
Motor  aphasia,  97,  103,  105,  440 
Motor  areas,  localisation  of,  4-6 
Motor   centres   in    cerebellar    cortex, 

24,  25 
Motor  cortex,  lesions  of,  6,  9,  19 
Motor    functions,     investigation     of, 

24,  50,  206 
Motor  nerves — 

fibrillary  tremors  in  paralysis  of, 

80 
regeneration  of  fibres,  232 
Motor  neurones,  upper  and  lower,  27, 

213 
Motor  paralyses,  206-218 

functional  or  organic,  210 
lower  neurone  type,  28,  206-221  ; 
distinguished  from  upper 
neurone  type,  213 
distinguished  from  anterior 
cornual  and  nerve-root 
lesions,  222-5 


Motor  paralyses  {continued) — 

distingtiished     from     cauda 

equina  lesions,  234-6 
Landry's  paralysis,  222,  233, 

326,  349 
level  of  lesion,  diagnosis  of, 

222 
from     multiple     peripheral 

lesions,  228,  233 
muscles,    affections    within, 

235 
postures  in,  267 
plantar  reflex  in,  213,  319 
sensory  phenomena  in,  222 
recurrent    and    transient,     248- 
256 
Eulenberg's  disease,  250 
family     periodic     paralysis, 

253 
in  general   paralysis   of   in- 
sane, 254 
in  hysteria,  255 
intermittent  limp,  251 
in  minor  epilepsy,  255 
myasthenia  gravis,  248 
myotonia  atrophica,  251 
occupation  neuroses,  253 
sign  of  disseminated  sclero- 
sis, 256 
in  tabes,  255 
tetany,  264 

Thomsen's  disease,  250 
upper    neurone    type,    28,    215- 
221;  bilateral,  218  distin- 
guished  from  lower  neu- 
rone type,  213-5 
exaggeration  of  deep  reflexes 

in,  329 
level  of  lesion,  diagnosis  of, 

214-221 
postures  in,  270-1 
unilateral,  215-8 
Motor     points,      397-8  ;      diagrams, 

391-7 
Miiller,      non-striated      muscle      of, 

paralysis,  337 
Muscles,  atrophy  of — 

causation,     28,     222,     224, 

290 
fibrillary  tremors  in,  80 
in  hemiplegic  arthritis,  314 
in  hysteria,  382 
idiopathic.     See  Myopathy 
in  neuritis,  227 
peroneal  type.  Tooth's,  225 
progressive  (chronic  anterior 
poliomyelitis),   80,   224-5, 
326,  402 
varieties  of,  225,  246-7 
dystrophy  of.     See  Myopathy 
•  electrical     reactions,      395-396 ; 
tests  for,  392 
fatigue-paralysis,  in  myasthenia 
gravis,  111 


468 


INDEX 


Muscles   (continued) — 

hypotonia,  87,  259,  263,  276-8 
motor    palsies    from     affections 

within,  255 
motor    points,    Erb's    diagrams, 

391-397 
non-striated      involuntary,      re- 
flexes of,  316,  330 
sensation,  active,  190 
sensibility  to  pressure,  194 
sensory  fibres  from,  18 
testing,  in  motor  paralysis,  206- 
209 
Muscle-spindle,  a  trophic  centre,  28 
Muscular  analgesia  in  tabes,  194 
Muscular  cramp,  254 
Muscular  localisation  in  cervical  en- 
largement, 34 
in  lumbo-sacral  cord,  34 
"Muscular    sense,"    definition,     190, 

194 
Musculo-spiral    nerve,    paralysis    of, 

28,  269 
Mutism,  hysterical,  116,  364,  387 
Myalgia,  181,  182 
Myasthenia    gravis.     111,     135,    248, 

400 
Myasthenic  reaction,  400 
Myatonia  congenita,  278 
Mydriasis,  128 

Myelitis,  54,  221,  298;  fig.,  299 
Myoclonus,  80-83;  diagram,  81,  82 

nystagmus,  83,  134 
Myoclonus  epilepticus  (Unverricht's), 

fig.,  81,  82 
Myoidema,  208 
Myokymia,  80 
Myopathy — 

atrophic  type,  237,  242-6 
diagrams  of  cases,  236-246,  287 
atrophy  of  nuclear  origin  distin- 

gxiished  from,  236-7 
Erb's  juvenile  type,  242—3 
facio-scapulo-humeral  type,  110, 

155,  238,  242,  244 
gait  and  posture  in,  286-7 
pseudo-hypertrophic  type,  237-9 
Myosis,  128,  339 
Myositis,  137,  194,  235 
Myotomes,  33 
Myotonia  atrophica,  251 
Mj'otonia  congenita  (Thomsen's  dis- 
ease), 250,  400 
Mj^otonic  reaction,  400 
Myx oedema,  427 

N^vi,  cutaneous,  301 
Nails,  trophic  changes,  306 
Narcolepsy,  64,  428 
"  Narcosis,  traumatic,"  55 
Nasal  crises,  119 
Nausea.     <Sie  under  Vomiting 
Neck,  motor  points  (Erb's  diagram), 
391 


Nephritis,  lumbar  puncture  for,  417 
optic  neuritis  in,  125 
uraemic  fits  of,  62,  70 
Nerve  areas,  trophic  changes  in  skin 

and  hair  over,  296-298 
Nerve-cells,  anatonay  of,  1 
"  Nerve  deafness,"  157 
Nerve  fibres — 

afferent,  influence  on  tissue  nutri- 
tion, 290 
motor,  6-9,  28,  30 
physiology  of,  2 
sensory,  8,  28,  31 
Nerve  plexus.     See  Plexuses 
Nerve  roots.     See  Spinal  Nerves 
Nerves.     See  under   Cranial,   Motor, 
Peripheral,    Spinal,   also   names    o/ 
particular  nerves 
Nervous  system, anatomy  and  physio- 
logy of,  1-47 
scheme  for  rovitine  examination 
of,  49-51 
Neuralgia — 

blanching  of  hair  in,  305 
brachial,  184 
coccygodynia,  181 
hyperaBsthesia  in,  197-198 
mammary,  182,  365 
meralgia  paraesthetica,  186 
post-herpetic,  297 
sciatic,  185,  320 
"  tender  points,"  180,  185 
trigeminal,  180 
Neurasthenia,  52,  54,  356-8 

causes  and  diagnosis,  356-7 
deep  reflexes  exaggerated  in,  32-7 
distinguished  from  hysteria,  355 
headaches  associated  with,  177 
mydriasis  in,  128 
toxic,  356-358 
traumatic,  182 
Neuritis — 

alcoholic,   51,    198  ;     diagram   of 

case,  233 
arsenical,  302,  300 
brachial,  diagram  of  case,  295 
diabetic,    perforating   ulcers   in, 

295 
hypertrophic  interstitial,  226 

ataxia  in,  261 
lead,  233 
leprous,  295 

loss  of  deep  reflexes  in,  326 
multiple  or  peripheral,   51,  188, 
194,    197-198,   205,   286,   306, 
330 
optic.     See  that  title 
post-diphtheritic,  110,  130,  155 
retro-bulbar,  125 
sciatic,   186 
Neuro-fibromata,  188,  303 
Neuromimesis,  355 
Nevirones — 

cerebello-dentate,  29 


INDEX 


469 


Neurones  (continued) — 

cortico-bulbar,  110,  112 

dentato-thalamic,  29 

lower  motor  (spino-muscular), 
27  ;  lesions  of,  28,  211-2.  See 
also  Motor  Paralysis,  Lower 
Neurone  type 

sensory  lesions  of,  28 

spino-cerebellar,  29 

thalamo-cortical,  29 

upper  motor  (cortico-spinal),  27  ; 
lesions   of,   28,   215.     See  a.  so 
Motor  Paralysis,  Upper  Neu- 
rone type 
Neuroses — 

hysteria,  361-388 

neurasthenia,  355-358 

psychasthenia,  358-360 
Nicotine  poisoning,  tremors  of,  84. 

See  also  Tobacco 
Nightmares,  429 
Noguchi's  test  for  globulin,  409 
Nuclear  ophthalmoplegia,  139 
Nuclei — ■ 

ambiguus,  164 

auditory,  39,  157 

bulbar,  110,  112 

caudate,  6,  42 

cerebellar,  21,  24 

cerebral  motor,  23 

cuneate,  15,  18 

Deiters',  21-26 

dentate,  21 

Edinger-Westphal,  126 

emboliformes,  21 

globosi,  21 

glosso-pharyngeal,  148,  155 

gracile,  15,  18 

hypoglossal,  148,  170 

lenticular,  6;    lesions,  113 

medullary,  15,  110' 

ocular,  21,  25,  86,  126 

red,  diagram,  23 ;  lesions,  86, 
139,  217,  265,  446 

Sixth  cranial  nerve,  10,  140 
Nyctalopia,  120 
Nystagmoid  jerks,  134,  152 
Nystagmus,  50,  85,  133-134 

aural  or  vestibular,  136 

cerebellar,  25 

facial,  89 

miner's,  133 

myoclonus,  83,  133 

reflex  (optic,  vestibular),  138 

rhythmic,  133 
oscillating,  133 

Obsessions  of  psychasthenia,  359 
Occupation  neuroses,  92,  253,  264, 
Ocular  headaches,  176 
Ocular  paralysis.     See  under  Paralysis 
Ocular      symptoms      in      Raynaud's 

disease,  35^ 
Ocular  vertigo,  161 


Oculo-pupillary     fibres    of     cervical 
sympathetic,     335 ;     paralysis    of, 
337  ;    diagram,  336 
Oculo-motor     (Third)     nerve.        See 

vnder  Cranial  Nerves 
(Edema,  acute  angio-neurotic,  352 
blue  hysterical,  387 
in  cavernous  sinus  thrombosis,  46 
(Esophagus,  hysterical  spasm  of,  385 

reflected  pains  of,  182 
Olfactory  nerves,  118;  path  of,  36 
Olivary  body,  16,  24 
Olivo-ponto -cerebellar  atrophy,  263 
Ophthalmoplegia,  126-7 

nuclear  (internal,  external, total), 
139;    tremor  in,  139 
Ophthalmoscopic    examination,     49, 

125,  175 
Opisthotonos,  68 
Opium  poisoning,  coma  of,  61 
Oppenheim's  reflex,  320 
Optic    atrophy,    123,    125,    128,    129, 

447 
Optic  chiasma — 

course   of    visual  fibres    in,    37  ; 

diagrams,  38,  124 
lesions  at  or  behind,  123-5,  130, 
447 
Optic  nerve,  37,  119 
Optic  neuritis,   125 

in  diagnosis  of  coma,  61 
headaches  with,  diagnosis,  175 
of  intra- cranial  tumour,  435,  441 
lumbar  puncture  to  reheve,  416 
Optic  radiation,  37,  188 
Optic  thalamus — 

lesions    of,    86,    174,    200,    216, 

443 
micturition  centres  in,  332 
reflex  centre  of  emotion,  444 
sensory  fibres  of,  16,  19,  444 
visual  fibres  in,  37 
Orbicularisoculi  (palpebrarum),  homo- 
logous with  branchial  arch  of  fish, 
141  ;    innervation,  140 
Orbital     muscle     of     Miiller,      335  ; 

diagram,  336 
Orthostatic  albuminuria,  347 
"  Osseous  sense,"  105 
Otic  ganglion,  148  ;    diagram,  142 
Otitis  media,  156-7 

vertigo  from,  161 
Ovarian  disease,  headache  from,  176 
"  Ovarian  tenderness,"  366 

Pain — 

course  of  fibres  subserving,  13-21 
diagnosis  of  cause,  173 
headache,  174-180 
hysterical,  189,  365 
in  limbs,  184  ;    bilateral,  187 
loss  of  sense  of,  21,  148-150,  204 
paroxysmal  spontaneous,  188 
reflected,  182 


470 


INDEX 


Pain  (continued)  — 
root,  187 

tests  for  sense  of,  191-205 
in  trigeminal  area,  179-180 
in  trunk,  180-184 
Palate,  soft — 

heini-atrophy,  147 
innervation,   143,  152,  163 
paralysis,    bilateral,     110;      uni- 
lateral, 164,  171 
reflex  movement,  317 
Pallsesthesia,  195 
Palpebral  aperture,  widening  of,  150, 

345 
Palsies.     See  Paralysis 
Panatrophy,  local,  304 
Pandiculation,  88 
Paracousis,  157 
Paresthesia,  50,  198,  201 
definition  of  term,  195 
hysterical,  375 
mapping  out  areas  of,  192 
Paradoxica-1  flexor  reflex,  319;  pupil- 
lary reaction,  130 
Paragraphia,  103 
Paralysis — 

alcohoUc,  155,  205,  233 
alternate  or  crossed,  10,  50,  209, 

216-7,  451-2 
atrophic  changes  in,  307-9 
Brown-Sequard,      13,      19,     195, 

201-2,  218,  220 
bulbar.     Sez  that  title 
of  cervical  sympathetic,  337-9 
cranial  nerves,  118-172 
crossed,  10,  50,  209,  216,  451 
facial,    110,    140,    148-155,   217  ; 

bilateral,  154  (diagram) 
family  periodic,  253,  327,  351,  400 
Fifth  nerve,  145-6 
glosso-labio-laryngeal.     See  Bul- 
bar Palsy 
glosso-pharyngeal,  163 
hypoglossal,  110,  147,   170,  171 
hysterical,    248,    256,    273,    274, 
380;  diagrams,  283,  362,  369- 
373,  380-1,  383 
infantile,   224,  272,  294,  307 
ischsemic,  236 
Landry's,  222,  233,  326 
laryngeal,  organic  and  functional 

(diagrams),  165-7 
Motor.     See  Motor  Paralyses 
motor    and    sensory    combined, 

219,  228,  330 
musculo-spiral  (diagram),  269 
myasthenia  gravis.     See  that  title 
ocular,  rheumatic,  137 
infra-nuclear,  138 
from    lesions    of    individual 

nerves,  130,  135-140 
nuclear  lesions,  139-140 
supra-nuclear,  137-8 
palatal,  95,  ]   0-1,  152,  164-5 


Paralysis  (continued)  — 

peripheral   motor  nerve  lesions, 
electro-prognosis  of,  402 

post-diphtheritic,  95,  110,  155 

in  tumours,  439-441 
Paralysis  agitans — 

articulative  difficulties  in,  114 

bilateral,  115 

diagrams  of  cases,  85,  288,  289 

Parkinsonian  mask,  115,  287 

posture  and  gait  of,  286-9 

rigidity  of,  84 

tremor,  84 
Paramyoclonus      multiplex      (Fried- 
reich's), 80-3  ;    diagram,  82 
Paramyotonia  congenita  (Eulenberg's 

disease),  250 
Paraphasia,  101 
Paraplegia — 

bed-sores  in,  298 

brachial  and  crural,  209 

chronic,  trophic  changes  in  nails, 
306 

definition,  209 

gait,  281-2 

hysterical,  274,   282,  283,  362-3 

(figs-) 
pure  motor,  221 
spastic,  53,  212,  219,  260,  282 
Paraplegia  dolorosa,  187,  188 
Para-sympathetic  fibres,  334 
Parathyroids,    tetany    from    extirpa- 
tion of,  77 
Parkinsonian  mask,  115,  287 
Parosmia,  49,  118-9 
paroxysmal,  119 
Patient,  examination  of,  48-54 
Penis,  analgesia  of,  in  tabes,  204 
Pericarditis,  reflected  pain  in,  182 
Perimeter,  use  of,  121,  374 
Periostitis  of  skull,  175 
Peripheral   irritation,    reflex    convul- 
sions from,  73 
Peripheral  nerves — 

cutaneous  areas,  32 
lesions — 

anaesthesia,  204 

ataxia,  259 

mixed,  222,  229-232 

motor    paralysis,     209-210, 

222-223,  326,  402 
sensibility  and,  14-5 
paths  of  sensation  in,  15 
Peripheral     neuritis.     See     Neuritis, 

Multiple 
Peritonitis,  194,  346 
Peroneal  muscular  atrophy,  226 
Personality,  alternating,  359,  378 
"  Petit-mal,"  65,  69,  255 
Petrous  ganglion  (diagram),  14^ 
Pharyngeal  reflex,  317 
Pharynx — 

anaesthesia,  56 

innervation,  163;  paralysis,  163 


INDEX 


471 


Pliobifc,  300 
Pill-rolling  tremor,  288 
Pineal  l)Oc]y — 

tumoiu's  of,  445-0 
Pi t u i  tar y  body — 

anatomy  and  physiology,  25  0 
Pituitary  tumours,  123-4,  291-3,  425, 
447 
and  hemianopia,  123 
"  Planchette,"   sub-conscious  pheno- 
mena of,  378 
Plantar  reflex,   2,    28,    57,    01,    213, 
219,  317 
Babinski's  phenomenon,  318-320 
in  liysteria,  320-322,  384 
Pleurodynia,  181 
Plexiform  neuroma,  303 
Plexuses — 

brachial,  symptoms  in  division  of 

posterior  roots,  259 
cervical,  29,  141,  145 
cervico-brachial     and    branches, 

29,  30 
hypogastric    and  h?emorrhoidal, 

331 
lumbo-sacral,  29,  31 
solar,  disorders  associated  with, 
340-347 
Pneumonia,  loss  of  deep  reflexes  in, 327 
"Polar  reactions"  of  muscle,  398 etseq. 
Polio-encephalitis,  superior,  74 
Polio-myelitis,    acute.     See   Infantile 
Spinal  Paralysis 
chronic  anterior,  80,  225,  320 
Poly-aesthesia,  190 
Polyopia,  monocular,  370 
Polyuria,  hysterical,  380 
Pons — 

arterial  supply,  41 
cranial  nerves  (diagram),  119 
facial  nerve,  origin  in,  148 
hsemorrhage,  57,  59,  128 
lesions  of,    10,   53,   80,  152,   201, 

203,  217-8 
nuclei,  110,  139 
sensory  fibres,  coiu-se  in,  17,  18 
tumours  of,  440,  451  (fig.) 
Ponto-cerebellar  angle,  lesions  of,  203 

tumours  in,  449  (fig.) 
Ponto-spinal  tract,  13 
Popliteal    nerve,     external    gait     in 
paralysis,  287 
posture  in  paralysis,  209 
"  Port-\\dne  stains,"  301 
Post-diphtheritic  paralysis,  110,  155 
Posterior  cerebral  artery,  41 
Posterior  columns  of  cord,  lesions,  15— 

18,  195,  259,  284,  320,  329 
Posterior  fossa,  tumours  of,  175,  328 
Posterior    nerve    roots.     See    Spinal 

Nerves,  Roots 
Postures,  207-289 

cerebellar,  285-280 
erect  and  at  rest,  207 


Postures  {continued) — 

in  functional  disease,  274-277 
in  hysterical  fits,  08 
in  organic  disease,  270,  270 
Pot  belly,  240,  287 
Preacher's  hand,  271 
Pregnancy — 

pseudo-,  385 
tetany  in,  79 
Pressure — 

blood,  in  coma,  55 
intra-cranial,   01,    71,    175,    320, 
408,  427;   lumbar  puncture  in 
relief  of,  415 
intra-thecal,  400 
labyrinthine,  103 
Pressure-pain,  13 
Pressure-sense,  192,  194 
Progressive    muscular    atrophy,    80, 

224-5,  320,  402 
Progressive      neuritic      amyotrophy 

(Charcot  and  Marie),  220 
"  Pronation  phenomenon  "  in  hemi- 
plegia, 214 
Proptosis,  40,  51 
Protopathic  cutaneous  sensibility,  14  ; 

loss  of,  204  ;    recovery  of,  232 
Pseudo-angina,  182,  384 
Pseudo-appendicitis,  380 
Pseudo-bulbar  paralysis,  113,  218 
Pseudo-hspmatemesis,  380 
Pseudo-hsemoptysis,  380 
Pseudo -hypertrophy,  237-9  (figs.) 
Pseudo-memories,  51 
Pseudo-pregnancy,  385 
Pseudo-ptosis,    51,    337,    339,    343  ; 

hysterical,  130;  diagram,  382 
Pseudo -tumour  cerebri,  453-4 
Psychalgia,  305 
Psychasthenia,  71,  358-300 
imperious  acts  in,  300 
obsessions  in,  359-300 
phobiae  of,  300 
stigmata,  300-301 
Psychic  epilepsy,  09 
Pterygooid  muscle,  external,  action  in 
congenital  ptosis,  141 
paralysis  of,  145 
Ptosis,  135,  382 
bilateral,  445 
congenital,  140 
hysterical,  137,  382 
pseiido-.  See  above,  Pseudo-ptosis 
Puerperal  eclampsia,  70,  417 
Pupil!  ary  reflex.  See  under  Reflex,  light 
Pupillary  unrest,  129 
Pupils — 

Argyll-Robertson      phenomenon 

in,  127,  129 
contraction — ■ 

in     affections     of     cervical 

sympathetic,  337 
in  opium  poisoning,  00 
in  pontine  hsemorrhage,  59 


472 


INDEX 


Pupils  [continued) — 

dilating    fibres,    course    of    (dia- 
gram), 127,  142,  335 
dilatation  of,  57,  62,  128,  135 
examination  of,  50,  128 
irregularity  in  shape,   57  ;    diag- 
nostic significance,  128,  345 
light  reflex.     See  under  Reflexes 
motor  innervation,  126 
painful     stimulation     of     neck, 

reaction  to,  130 
paradoxical  reaction,  130 
psychical  dilatation,  130 
reaction  to  accommodation,  130 
size,  variations  in,  128 
Pyramidal  cells,  6 
Pyramidal  tract — 

course,  11,  27  ;  and  diagram  of,  7 
lesions  of,  9-11 
gait  in,  281 
motor  paralysis  due  to,  86, 

217-8 
reflexes  affected  by,  318-319 
and  note,  327  ;  in  hysteria, 
384 

QxTADRANTiG  hemianopia,  37 
Quinquaud's    sign    of    chronic    alco- 
holism, 84 

Rabies,  76 

Rami  communicantes,  334-336 

Raynaud's  disease,  51,  53  note,   188, 

299,  348-350 
Reactions  of  degeneration,   28,   208, 

213,  400-2 
von  Recklinghausen's  disease,  302-3 
Recti  muscles  of  eye  (diagrams),  126, 

131-142 
Recurrent  and  transient  motor  para- 
lysis, 248-256 
Recurrent  laryngeal  palsy,  1 64-8 
Recurrent  utterances,  106 
Red  nucleus,  connections  (diagram), 
12    23 
lesioAs,  86,  139,  265,  446 
Reeling  or  titubating  gait,  263,  285 
Reflected  pains    of   visceral    disease, 

182 
Reflex  arc,  2,  28,  129,  318 
Reflex  convulsions,  74 
Reflex  spasms,  92 
Reflexes,  50,  316-333 
abdominal,  317 
anal  — 

internal,  330,  332 
superficial,  317,  319 
Babinski's   extensor   plantar  re- 
flex, 317-8 
Brissaud's,  318 
bulbo-cavernosus,  317,  320 
ciHo-spinal,  51,  330,  338,  340 
conjvmctival,  150,  317 
conscious  and  unconscious,  2,  4 


Reflexes  {continued) — 

cortical  and  spinal,  318,  319 
cremasteric,  317,  320 
dartos,  333,  419 

deep  or  tendon,  50,  316,  321-329 
in  ataxic  conditions,  259 
after  epileptiform  fits,  68,  72 
exaggerated,  19,  HI,  327 
loss  of,  320,  326 
in  upper  and  lower  neurone 
motor  paralyses,  28,  213 
effect  of  spinal  injuries  on,  20, 

219 
epigastric,  317 
genital,  4,  330 
gluteal,  317 
in  hysteria,  64,  68,  383 
jaw,  321 
light,  2,  129,  330 

in  hysteria,  64,  68,  383 
loss  of,  126,  129,  130 
path  of,  126  ;  diagram,  127 
of  non-striated  muscles,  330 
Oppenheim's,  320 
optic.     See  above  (Light) 
palatal,  317 
paradoxical  flexor,  319 
pharyngeal,  317 
plantar,  2,  28,  57,  61,  213,  219, 

317,  318-322 
pupillary.     See  above  (Light) 
rectal,  330 
scapular,  317 
scapulo-humeral,  321 
scrotal,  330,  333 
sexual,  4,  330 
superficial  (or  skin),  50,  57.  316- 

321 
uterine,  330 
vomiting,  4 
Pvenal    disease.     See    under    Kidney 

and  Nephritis 
Restiform  body,  24,  39 
Retina,  37,  129 

Retinal    cedema,    diagnostic    signifi- 
cance, 59 
Retinitis  pigmentosa,  120 
Retro-bulbar  neuritis,  125 
Retrograde  amnesia,  55 
Retro  -  quadrigeminal       hemianopia, 

light  reflex  in,  130 
Rheumatic  myositis  of  external  ocu- 
lar nuiscles,  137 
Rickets,  convulsions  and  tetany  due 

to,  73,  77 
Righthandedness,  38,  40 
Rigors,  79 

Rinne's  test  for  hearing,  156 
Rolando,  fissure  of,  9,  19 
Romberg's  sign  in  tabes,  258,  260 
Root-areas,  diagrams  of,  35 
Root-lesions,  29,  195,  222-236 
Root-pains,  180-181,  187 
Rosenbach's  sign  of  hemiplegia,  57 


TNDEX 


473 


Rotatory       movements,       cerebellar 
stimulation  and,  25 
in  intra-cerebellar  growths,  450 
Round-worms,    convulsions    due    to, 

74 
Rubro-spinal  tract,  13,  8G,  139,  265 

loss  of  function,  327,  445-6 
Rupophobia,  360 

Sacral  pain,   184 

Sacral  plexus,  29 

Sacral  segments,  lesions,  320 

Sacro-coccygeal  root-areas  (diagram), 

35 
Saliva,  irregularity  in  flow  of,  150-2 
Saltatory  spasms,  94 
Scapular  reflex,  317 
Scapulo-humeral  reflex,  321 
Sciatic  nerve,  paralysis  of  (fig.)j  231 
Sciatica,  185 
Scissor  gait,  281 
Scleroderma,  300 
Sclerosis — 

amyotrophic  lateral,  80,  111,  221, 
225,  326 

disseminated.     See  Disseminated 
Sclerosis 

multiplex  dolorosa,  181 

postero- lateral,  285 

primary  lateral,  220 
Sclerotomes,  33 

Scotomata,  central,  121,  120  ;   of  mi- 
graine, 178 ;    for  red  and  green  in 
tobacco  amblyopia,  120 
Scrotal  reflex,  330,  333 
"  Seelenlamung,"  Nothnagel's,  382 
Segmentation    of    spinal    cord    (dia- 
grams), 30-3 
Semicircular  canals,  disease  of,    158- 

163 
Senile  tremor,  84 
Sensation — 

clinical  investigation  of,  190-2<>o 

paths  of,  15 

muscle -active,  190 

physiology  of,  13-5 

return  after  mixed  nerve  para- 
lysis, 232 
Senses,  special,  paths  of,  36-40 
Sensibility,  kinds  of,  13 
Sensory  fibres,  position  of,  8,  9 

fits,  73 

functions,  50 

paths,  13-21 
Serratus  magnus,  paralysis  of,  232 
Sewer-gas  poisoning,  293 
Sexual  reflex,  4,  330 
Shivering,  79 
Shoemakers'  tetany,  77 
Side-gait  ("  Flankengang  "),  283 
Sight.     See  Vision 
Skew  deviation  of  eyes,  138 
Skin- 
areas  of  peripheral  nerves,  32 


Skin  {continued) — 

hysterical  affections,  386-7 
pigmentary  changes,  301-3,  347 
sensibility  of,  14,  15,  191-3 
loss  of,  21,  204 
recovery  of,  230 
trophic  changes,  294-303 
Sleep,  disorders  of,  423-433 
pathological,  426 
physiology  of,  423-6 
Sleeping  sickness,  428 

parasites  in  cerebro-spinal  fluid, 
411 
Smell,  disorders  of,  49,  73,   118,  119, 
145  ;  hysterical,  367,  373  ;  olfactory 
path,  36  ;  tests  for  sense  of,  118 
Sneezing  in  parosmia,  119 
Snellen's  types,  119 
Somnambulism,  377,  426,  429 
Spasms,  habit,  90 

hysterical,  94,  379,  387 
reflex,  92 
saltatory,  94 
See  also  Tics 
Spasmus  nutans,  85 
Spasticity,  28,  213 
Special  senses,  paths  of,  36-9 
Speech — 

articulation  distinguished   from, 

109 
auditory  origin  of,  97 
cortical  centres  for,  96-100 
disorders,  in  diagnosing  nervous 

disease,  52-4 
hysterical  affections,  364 
loss  of — 

aphasia.     See  that  title 
articulation,     defects.       See 

Articulation 
causes,  classiflcation  of,  95 
vocal   and  consonantal  ele- 
ments in,  109 
Sphincter     ani,     externus,     34,     317, 

320;  internus,  330,  332 
Spina  bifida  occulta,  295,  304 
Spinal  accessory  nerve,  164 
Spinal  anaesthesia,  418-422 
after-effects  of,  420 
contra-indications,  421 
Spinal  cord — 

arterial  supply,  44 
cervical  region- 
lesions  in,  128,  181,  209,  218 
muscular  localisation  in,  34 
Clarke's  column,  19 
coccygeal  segment,  184,  320 
combined   degeneration  of,  260, 

329 
endogenous  tracts,  19 
grey  matter,  focal  lesion  of,  326 
lateral  column,  15,  16,  329 
lesions  of — 

ansesthesia  in,  201-3 
bladder  trouble  due  to,  331 


474 


INDEX 


Spinal  cord,  lesions  of  (continued) — 
complete     and    incomplete, 

201,  218-9 
hemi-section  of,  11,  19,  195, 

200-1,  218 
paralysis  dxie  to,  11,  19,  219 
posterior  roots  and  columns 

of,  13-21,  259-260 
in     pyramidal      tract.     See 

Pyramidal  tract 
rectal     incontinence     from, 

331 
root  pains  due  to,  187 
symptoms  of,  19 
trans- section,    complete    of, 

201,  219,  326,  327,  329 
unilateral,  218 
lumbo-sacral  region,  i^ee  Lumbo- 
sacral cord 
malignant  growths  in,  411 
micturition  centres  in,  331-2 
paths  of  sensation  in,  15 
posterior  cokimns,  15-8,  195,  259, 

284,  326,  329 
relations  with  vertebral  column 

(diagram),  404 
root  irritation  from  diseases  of, 

187 
segments  (diagram),  30-5 
sub -acute     combined     degenera- 
tion, 260,  329 
tracts  of,  10-3,  17 
tumours,      intra-      and      extra- 
medullary,  181,  219;    cerebro- 
spinal fluid  in,  411 
vaso-motor  centres,  diseases  of, 
350 
Spinal  nerves — 

anterior  roots,  2,  27  ;    lesions  of, 

27-35,  222-4 
mixed  motor  and  sensory  para- 
lysis due  to,  218-9,  228,  329 
motor  paralysis  due  to,  27-35 
posterior  roots — ■ 

cutaneous  areas,  32 
distribution,  27-35 
inflammation      of     ganglia, 

187,  296-8 
irritation,  180,  187,  196-8 
lesions  of,  27-35,  259,  327 
sensory  path  through,  1 5 
Spino-muscular   motor   nem"one    les- 
ions.    See  Motor  Paralyses 
Spino-thalamic  tract,  16 
Splanchnic  disease,  346-7 
Squint,  50,  131 

Stammering,  115  ;    hysterical,  364 
Stellwag's  sign  of  exopthalmic  goitre, 

346 
Stereognostic  perception,  195,  443 
Sterno-mastoid,    paralysis    of   (figs.), 

91,  168 
Stokes-Adams'  syndrome,  62,  74 


Stomach — 

dilatation  of,  77,  164,  347 
hysterical  rumblings  in,  385-6 
reflected  pains  of,  182 
Storaine  as  anaesthetic,  418 
Strumpell's  tibialis  phenomenon,  214 
Strychnine  poisoning,  75,  327,  418 
Stupor,  55 

Sub-cortical  cerebral  tumours,  73 
Sub-cortico  spinal  tracts,  11,  13 
Sunstroke   and    alcoholics,    63  ;    and 

coma,  63,  177 
Supinator  jerk,  321,  325 
Supinator  longus,  paralysis  of,  30 
Sweating — 

abnormalities,  due  to  nerve  dis- 
order, 51,  343-4,  353 
centre,  353 
cervical   sympathetic   connected 

with,  335,  338,  339,  343 
of  hysteria,  386 
in  Meniere's  disease,  162 
Sylvian  fissvire,  9,  39,  96 ;  arteries  of, 

43 
Symmetrical  gangrene,  349 
Sympathetic  nervous  system — 

course  and  distribution,   1,  334 
lesions  of,  336-344 
thoracico-abdominal,  diseases  of, 

347,  348 
visceral    reflexes    controlled    by, 
316,  330-3 
Syncope  distinguished   from  "  petit- 

nial,"  69 
Syphilis — 

cerebro-spinal  fluid  in  diagnosis 

of  lesions,  414-5 
diagnosis  of,  452 
epilepsy  secondary  to,  71,  72 
irregularity  of  pupils  in,  71,  128 
meningitis  of,  180 
palatal  perforation  from,  110 
Third    nerve    palsy    from    (fig.), 
135 
Syringobulbia,  202 
Syringomyelia — • 

arthropathy  (diagrams),  203,  221, 

309,  313 
cerebro-spinal  fluid,  409 
claw-hand  in,  271 
dissociated  anaesthesia,  196,  202, 

221 
exaggerated  deep  reflexes,  327 
fibrillary  tremors,  80 
loss  of  deep  refiexes  in,  326 
ocular  symptoms,  128 
pain  from,  173 
perforating  ulcers  in,  295 
spontaneous  fractures  in,  309 
thermo-ansesthesia  and  analgesia, 

(diagrams)  202-3,  310 
trophic    changes  in  joints,   221, 
309-13 


INDEX 


475 


Tabes — 

ansBsthesia  of,  203-5,  332  ;  dia- 
gram, 201 

ankle-jerks,  325 

anosmia,  118 

Argyll-Robertson  phenomenon, 
127, 129 

arthropathy,  diagnosis  of  eases, 
308-14 

ataxia,  258-66 

biilbo-cavernosus  reflex,  loss  in, 
320 

cerebro-spinal  fluid  in  diagnosis 
of,  414-15 

crises  in,  183,  347 

delayed  sensation  in,  193 

gait  in,  284-5 

girdle  pains  in,  181 

hair,  loss  of,  (fig.)>  305-6 

hypersesthetic  areas,  186 ;  dia- 
gram, 204 

hypotonia  in,  276-7 

involuntary  movements,  89,  308 

(%•) 

joint  and  kinesthetic  senses, 
loss  of,  194 

laryngeal,  112 

lightning  pains,  187,  197 

light  reflex,  loss  of,  127,  129,  313 

muscular  and  tendinous  anal- 
gesia, 194,  204 

myosis,  128 

nasal  crisis,  119 

optic  atrophy,  primary,  125 

perforating  ulcers,  295 

pupils,  irregularitv  of,  128 

reflexes,  128-130,"  320,  326,  330 

spontaneous  fractures,  309 

sudden  falling  in,  255 

trophic  changes,  295-96,  347 

vibration  sense,  loss  of,  195 
Tactile  sense,  13-15,  19 

loss  of,  21,  191 
Talipes  equino-varus,  226 
Taste,  cortical  centre  for,  39 

coarse  of  fibres  serving,  39,  143, 
155,  163:    diagrams,  142,  151 

disorders  of,  144-5,  155,  163; 
hysterical,  367,  373,  374 

in  Fifth  nerve  palsy,  143 

tests  for  sense  of,  144 
Tear  secretion,  paralysis  of,  145 
Tecto -spinal  tract,  13 
Tegmental  lesions,  86,  446 
Temperature  in  cerebralhaemorrhage, 

58 
Temperature    sense,    fibres    serving, 
15-20 

tests  for,  190,  192 
Temporal  lobe,  disease  of,  40,  72,  441 
Tetanus,  75,  327,  417 
Tetany,  77,  254 

and  cataract,  77 

Chvostek's  sign  of,  77 


Tetany  (continued) — 

endemic,  of  shoemakers,  77 

from  extirpation  of  parathyrf)ids, 
77 

Erb's  sign  of,  77 

Trousseau's  sign  of,  77 
Thalamic  syndrome,    174,    196,    200, 

216,  444-5 
Thalamo-cortical  pathway,  8 
Thecal  puncture,  404 
Thermic  nystagmus,  133—4 
Thigh,  motor  points  (Erb's  diagrams), 

395,  397 
Thirst,  cortical  centre  for,  40 
Thomsen's    disease    (Myotonia    con- 
genita), 250,  400 
Thoracic    nerves,    lesions    producing 

ocular  symptoms,  337 
Thrombosis,  bilateral,  of  corpus  stria- 
tLun  syndrome,  293 

of  cavernous  sinus,  46 

cerebral,  41,  45-47,  59,  98,  101, 
159-160, 176,  408 

spinal,  45,  53 
"  Tibialis  phenomenon,"  214 
Tic  douloureux,  93,  180 
Tics,  90-92,  116 

cUstinguished  from  chorea,  91 

hysterical,  360 
Tinnitus,  150,  157,  162,  175;  lumbar 

puncture  to  relieve,  417 
Tobacco  amblyopia,  120,  122,  125 
Tongue — 

ataxy  of,  112 

biting,  in  epilepsy,  67 

hemi-atrophj',  146,  171 

innervation,  143,  163,  170,  335 

paralysis,  110,  170-1 

taste  fibres  to,  143,  152,  163 
Torcular  Herophili,  46 
Torticollis,  idiopathic  spasmodic,  91  ; 
labjTinthine,    92  ;     neuralgic,    92  ; 
professional,  92 
Touch.     See  Tactile  sense 
Toxicophobia,  360 
Trance,  hysterical,  64,  377 
Traumatic  cerebral  compression.  59 
Tremor,  83,  84-86 

Quinquaud's  sign  in  alcoholism, 
84 

senile,  84 

toxic,  84  ;    in  tumours  of  frontal 
lobe,  86 
Triceps  jerk,  321,  326 
Trichiniasis,  235 
Tricho-anfBsthesia,  191 
Trigeminal  nerve.  See  Cranial  Nerves 
Trigeminal  neuralgia,  179-180 
Trophic  functions,  50 
Tropho-neuros-s,  290-315 

bones  and  joints,  306 

generalised  trophic  disorders,  291 

skin  and  its  appendages,  294 
Trousseau's  sign  of  tetany,  77 


476 


INDEX 


Trypanosome    of    sleeping    sickness, 

411 
Tubercles  of  choroid,  125 
Tubercula  dolorosa,  188 
Tuberculin,      Calmette's      and      von 

Pirquet's  reactions,  453 
Tubercxilous  meningitis,  52,  175,  411, 

412,415 
Tumours — 

abdominal  phantom,  386 
diagnosis,  54,  434  ;    differential, 

219,  451-4 
intra-cranial,   72,    125,    160,    175, 
177-8,  425-7,  434-454 
Central  ganglia,  444 
Cerebellum,    157,    160,    178, 
264,  285  ;  ataxia  in,  263  ; 
extra-   and   intra-cerebel- 
lar,  447 ;  lateral  lobe,  448  ; 
middle  lobe,  450  ;  fits  due 
to,  65,  77,  450 
coma  in,  61 
Corona  radiata,  444 
Corpora  quadrigemina,  445 
Corpus  callosum,  445 
Crusta  of  crus  cerebri,  446 
diagnosis,  452-4 
and  drowsiness,  427 
epileptic  fits  from,   71,  436, 

438 
Fourth  ventricle,  452 
Frontal   region,    440 ;  anos- 
mia in,  441 ;  tremor  of,  86 
giddiness  in,  436 
headache  of,  175,  177-8,435 
hemianopia  from,  123 
Internal  capsule,  444 
Jacksonian  fits  in,  436,439, 

440 
Medulla  oblongata,  452 
mental  dulness  in,  436 
of  mid-brain,  126,  423-4 
Motor  cortex,  439 
Occipital  region,  443 
optic  neuritis,  125,  435 
Pineal  body,  445 
Pituitary,     123,     293,     425, 

447 
Pons,  451 
Post-central        convolution, 

442 
Postero-parietal  lobule,  443 
Post-frontal,  440 
Pre-central  (fig.),  438 
Pre -frontal,  440 
slowness  of  breathing,  437  ; 

of  pulse,  437 
Supra-marginal  and  angulas' 

convolutions,  442 
Temporal  lobe,  441 
Tegmental  region  of  crus  or 

Pons,  446 
Vermis,  450 
vomiting  in,  436 


Tumours  {continued) 

lumbar  puncture  for  inoperable, 

416 
pelvic,  186 

of     spinal     cord,      219  ;     differ- 
ential diagnosis,  219-220,  451 ; 
meningeal,  181,  186,  187 
Tuning-fork,  tests  for  hearing,  156 
Typhus  fever,  "  coma-vigil  "  of,  64 

Ulcers — 

perforating,  50,  296 

rodent,  282 
Ulnar  paralysis,  230 
Uncinate  gyrus.       See  under  Gyrus 

fits,  73,  441 
Unverricht's      family      myoclonus, 

diagram,  81-2 
Uraemia — 

coma  of,  62,  428 

convulsions,  70,  74 

Jacksonian  fits  in,  73 
Urine — 

in  alcoholic  poisoning,  62 

diabetic,  63 

dribbling  of,  332 

hysterical  incontinence  and  re- 
tention, 384 ;  suppression, 
386 

reflex  incontinence,  331 

retention,  331 

in  ursemic  coma,  62 
Urticaria    scripta,     352,     387  ;     dia- 
grams, 136,  387 
Uterine      disease,      headache     from, 

176 
Uterine  reflex,  330 

Vascxjlar  causes  of  insomnia,  430 
Vaso-constriction  in  sleep,  423-424 
Vaso-motor  neuroses,   347-354,  384- 

388 
Veins,  intracranial,  45-47 
Venereal  diseases,  questions  as  to,  49 
Ventral  longitudinal  bundle,  13 
Vermis,  21,  24,  25 

tumours  of,  450 
Vertebral  arteries,  41,  44 
Vertebral  column,  50  ;    diagram,  404 
Vertigo — 

ataxia  in,  263,  285 

causes,  158-163 

pathological,  159-161 
Vesical  reflex,  330 
Vestibular  nerve — 

connections  of,  40 

lesions,  138,  156 

tests  for  integritv,  133 
Vestibulo-spinal  tract,  13,  21,  24,  25 
Vibrant  electricity,  389 
Vibration  sense,  13,  20,  190,  195 
Vidian  nerve,  142 

Visceral   disease,    reflected   pains   in, 
182 


INDEX 


477 


Visceral  phenomena  of  hysteria,  384- 

386 
Vision- 
fibres  of,  path  of,  36-39 
field  of,  37,  49 

concentric  contraction,  123, 
442  ;  in  myasthenia,  250 
hysterical,      373  376;     dia- 
gram, 374-375 
measurement,  121-123 
hysterical  blindness.  375 
colour-vision,  373-375 
hyperesthesia ,  366-367 
Visual  acuitj',  tests  for,  118 
Visual  aphasia,  102-3,  105;  diagrams, 
96,  98 
centres  for,  37,  105 
cortical  and  sub-cortical,  37—39, 
definition,  102 

lesions  producing  (diagrams),  38, 
96,  102 
Visual  cortex,  36-39,  442 
Visual  hallucinations,  72,  444 
Visual  word-centre,  96,  100,  442 
Visuals  and  auditives,  98,  101 
Vocal  word  centre,  97,  441 
V.    Volkmann's    ischsemic    paralysis, 

236 
Vomiting,  4,  74,   152,  156,   159,   160, 
161,  175,  178 
cerebral,  436 
hysterical,  384-386 
reflex,  4 

Walking.     See  Gait 
Wallerian  degeneration,  27,  29 
Weber's  law,  194 


Weber's  syndrome,  10,  217,  446 

Weber's  test  for  hearing,  156 

Werdnig-Hoffmann  type  of  progres- 
sive muscular  atrophy,  225 

Werner's    "  memoria    technica,"    for 
false  images  (diagram),  132 

Wernicke's   hemiopic    pupillary    re- 
action, 130,  443 

Wernicke's    zone,    disintegration    of, 
105 

Whitlows,  painless,  203,  296 

Willis,  circle  of,  42 

Witches,  368 

Word -blindness.     See  Visual  aphasia 

Word-centre — 

aviditory,  96;   diagram,  98,  102 
visual,  96-97 
vocal,  96,  441 

Word-deafness.   See  Auditory  aphasia 

Word-swallowing,  91 

Wrisberg,  nervus  intermedins  of,  148, 
155 

Wrist  reflex,  321 

Writers'  cramp,  253,  264 

Writing,  motor  centre  for,  97 

X-KAYS  in  neurology,  389 
in  tumours,  437 

Yawning,  automatic  extensor  move- 
ments in,  88 
in  intra-cranial  disease,  437 
Yohiixibine  poisoning,  400 

Zacharias,  instanceof  motor  aphasia, 
104 


THE    END 


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